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- 1  '  ^'  I  r  r  i  r  V 


ACCIDENT  AND  INJURY 

THEIR  RELATIONS  TO  DISEASES 
OF  THE  NERVOUS  SYSTEM 


BY 

PEARCE  BAILEY,  A.M.,  M.  D. 

ATTENDING  PHYSICIAN  TO   THE   DEPARTMENT   OF   CORRECTION 

AND   TO   THE   ALMSHOUSE   AND    INCURABLE    HOSPITALS  ; 

ASSISTANT  IN  NEUROLOGY,   COLUMBIA  UNIVERSITY  ; 

CONSULTING   NEUROLOGIST    TO    ST.    LUKE'S 

HOSPITAL,   NEW   YORK   CITY 


NEW    YORK 
D.    APPLETON    AND    COMPANY 

1900 


Copyright,  1898, 
By  D.  APPLETON  AND  COMPANY, 


TO 

PROFESSOR   STARR, 

IN    GRATEFUL    RECOLLECTION 

OF    MANY    KINDNESSES. 


3 

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CD 

CD 


.'^  S 1  A  A  .R 


PREFACE. 

The  original  purpose  in  this  undertaking  was  to  furnish 
a  systematic  description  of  the  nervous  affections  which 
result  from  injury  and  fright,  and  which,  under  the  gener- 
ally familiar  term  of  "  the  traumatic  neuroses,"  exist  inde- 
pendently of  any  as  yet  demonstrated  lesion  in  the  nervous 
system.  These  disorders  are  of  sufficiently  common  oc- 
currence to  constitute  a  comprehensive  chapter  in  internal 
medicine,  and  they  have  obtained  a  position  of  legal  promi- 
nence from  the  frequency  with  which  they  are  associated 
with  questions  of  liability.  Yet,  in  spite  of  their  impor- 
tance, that  they  are  not  always  clearly  understood  by 
physicians  generally  is  shown  by  the  contradictory  views 
expressed  concerning  them  when  they  become  the  subjects 
of  litigation. 

While  it  can  not  be  denied  that  the  nature  of  the  trau- 
matic neuroses  is  still  in  many  respects  obscure,  sufficient 
evidence  as  to  their  causes  and  symptoms  has  now  accumu- 
lated to  permit  them  to  be  recognized  as  definite  clinical 
types,  and  to  be  diagnosticated  with  reasonable  accuracy. 
This  evidence  is,  however,  more  or  less  inaccessible  to  gen- 
eral readers,  existing  chiefly  as  scattered  monographs,  most 
of  which  are  in  foreign  languages.  No  single  book  has  at- 
tempted, in  recent  years,  to  present  in  detail  the  enlarging 
views,  and  the  deductions  from  them,  concerning  these  dis- 
orders. More  than  a  year  ago  it  appeared  to  the  writer 
that  an  embodiment  of  such  views  and  deductions,  together 


Vl  PREFACE. 

with  facts  of  personal  experience,  might  prove  of  service, 
not  only  to  practitioners  of  medicine,  but  also  to  those  whose 
interest  in  the  questions  involved  arises  from  legal  rather 
than  from  medical  reasons. 

This  task  was  accordingly  undertaken.  As  it  pro- 
gressed it  became  evident  that  a  treatise  on  the  traumatic 
neuroses  would  be  much  more  useful  were  it  preceded 
by  some  account  of  injuries  to  the  nervous  system  of  or- 
ganic character.  A  disease  can  only  be  diagnosticated 
as  functional  when  evidences  of  organic  lesion  are  absent, 
and  the  physician  to  recognize  the  one  must  be  able  to 
exclude  the  other.  Accordingly,  instead  of  proceeding  at 
once  to  the  delineation  of  neurasthenia,  hysteria,  and  allied 
conditions,  the  first  parts  of  the  volume  are  concerned 
with  the  simpler  methods  of  examination,  with  the  causes 
and  effects  of  acute  organic  injuries  to  the  nervous  sys- 
tem, and  with  a  consideration  of  in  how  far  accidents  may 
be  held  responsible  for  the  appearance  of  certain  chronic 
degenerative  diseases.  The  question  of  malingering  is  so 
intimately  connected  with  the  traumatic  functional  nervous 
disorders  that  its  description  also  was  deemed  essential. 
Treatment  does  not  properly  fall  within  the  scope  of  the 
work  as  indicated  by  the  title,  but  since  it  is  a  subject  of 
such  importance  the  few  words  regarding  it  may  be  found 
not  out  of  place. 

In  its  present  form  the  book  might  be  mistaken  for  a 
general  treatise  on  traumatic  diseases  of  the  nervous  system. 
So  comprehensive  a  purpose  it  can  not  aspire  to  fulfil.  It 
is  merely  an  attempt  to  present  the  views  which  seem  most 
tenable  as  to  the  part  played  by  injury  and  shock  in  the 
more  important  of  these  diseases.  The  writer  has  drawn 
freely  upon  the  works  of  Erichsen,  Page,  Charcot,  Oppen- 
heim,  Knapp,  Dana,  Gilles  de  la  Tourette,  Striimpell,  Heller, 
and  many  others,  for  which  he  desires  to  express  his  obli- 
srations.      His  warmest  thanks  are  due  to   Professor  Starr 


PREFACE 


VU 


,  for  kindly  suggestions  given  during  the  preparation  of  the 
manuscript,  and  for  his  permission  to  make  use  of  the  rich 
material  of  the  Department  for  Nervous  Diseases  at  the 
Vanderbilt  Clinic  ;  to  Dr.  V.  H.  Norrie  for  many  of  the 
photographs  ;  and  to  Mr.  I.  Strauss  for  help  in  correcting 
the  proofs  and  in  many  other  ways. 

Pearce  Bailey. 

60  West  Fiftieth  Street,  New  York, 
October  20,  iSg'j. 


CONTENTS. 


PAGE 

Introduction  : 

The  consideration  of  the  case i 

I. — Previous  history  of  the  patient 6 

II. — History  of  the  accident 7 

III. — Physical  evidences  of  predisposition  to  nervous  disease.  ii 

IV. — The  examination  for  the  actual  injury      .        .        .        .  18. 

PART   I. 

ORGANIC  EFFECTS  OF  INJURY  TO    THE  NERVOUS  SYSTEM. 

CHAPTER 

I. — Injuries  to  the  brain 46 

II. — Injuries  to  the  spinal  cord 68 

III. — Injuries  to  the  peripheral  nerves 97 

IV. — Ultimate  organic  effects  of  injury 119 

Epilepsy 126 

General  paralysis  of  the  insane 137 

Locomotor  ataxia .  151 

Progressive  muscular  atrophy 164 

Paralysis  agitans 178 

PART    II. 

FUNCTIONAL   EFFECTS   OF  INJURY. 

I. — The  nervous  disorders  w^hich  most  frequently  follow  rail- 
way AND   ALLIED    ACCIDENTS. — ThE  TRAUMATIC   NEUROSES      .           .  l86 

History 186 

Nomenclature       200 

Pathology 202 

^Etiology 203 

Symptoms 215 

II. — Traumatic  neurasthenia 226 

III. — Traumatic  hysteria 270 

IV. — Unclassified  forms 325 

ix 


X  CONTENTS. 

PAGE 

PART    III. 

Malingering 34i 

1.  Exaggeration  of  symptoms  actually  present       ....  347 

2.  Substitution  of  origin        .........  352 

3.  Simulation •  357 

PART   IV. 

Treatment  of  the  traumatic  neuroses 394 

Index  of  names 419 

Index  of  subjects 422 


LIST   OF   ILLUSTRATIONS. 


FIGURB  PAGE 

1.  Schweigger's  perimeter 24 

2.  Normal  field  of  vision 25 

3.  Hand  dynamometer  .         .         .........  29 

4.  Krauss's  plessimeter 38 

5.  Method  of  obtaining  triceps  and  supinator  jerks        .....  39 

6.  Jendrassik  method  of  obtaining  the  knee-jerk 40 

7.  Diagram  of  nerve  trunks  and  motor  points  for  the  muscles  (opposite)         .  43 

8.  Diagram  of  degenerative  electrical  reactions 44 

g.  Schematic  representation  of  the  cerebral  cortex  and  its  centers          .         .  50 

10.  View  of  the  right  cerebral  hemisphere        .         .         .         .         .         .         .51 

11.  Schema  of  cerebro-spinal  motor  path          .......  53 

12.  Schema  of  the  motor  neurons     .........  54 

13.  Photograph  showing  double  third-nerve  palsy    .         .         ,         .         .         .  58 

14.  Photograph  showing  palsy  of  the  sixth  and  seventh  nerves         ...  59 

15.  Same  patient 59 

16.  Section  through  the  back  at  the  ninth  thoracic  vertebra    ....  70 

17.  Crush  of  spinal  cord 72 

18.  Intradural  haemorrhage 73 

19.  Extradural  haemorrhage     . .73 

20.  Course  of  blood  in  hsematomyelia 74 

21.  Section  showing  hsematomyelia .         . 75 

22.  Sensory  distribution  of  spinal-cord  segments  (Starr) 91 

23.  Sensory  distribution  of  spinal-cord  segments  (Kocher)       ....  92 

24.  Anesthesia  chart.     Injury  to  eighth  cervical  segment         ....  93 

25.  Anaesthesia  chart.     Injury  to  fifth  lumbar  segment 94 

26.  Sensory  distribution  of  peripheral  nerves  (opposite)  .     '    .         .         .         .  106 

27.  'Begm.mxig  main  en  griffe no 

28.  Distribution  of  sensoiy  nerves  in  the  hand iii 

29.  Drop-wrist          .         . .  113 

30.  Deformity  of  the  back  in  syringomyelia 123 


xii  LIST   OF    ILLUSTRATIONS. 

FIGURE  PAGE 

31.  Acromegaly 125 

32.  Facial  expression  in  general  paresis .  139 

33.  Handwriting  in  general  paresis           ........  145 

34.  Charcot  joint      .          ...........  153 

35.  Attitude  of  static  ataxia      . 154 

36.  AnEesthesia  chart.     Locomotor  ataxia         .         .         .         .         .         .         -155 

37.  Field  of  vision.     Locomotor  ataxia    ........  160 

38.  Progressive  muscular  atrophy     . 174 

39.  Same  patient      ............  175 

40.  Facial  expression  in  paralysis  agitans  .         .         .         .         .         .         .180 

41.  Attitude  in  paralysis  agitans       . .  iSi 

42.  Attitude  in  traumatic  lumbago   .........  248 

43.  Field  of  vision.     Shifting  type  of  contraction     ......  255 

44.  Anaesthesia  chart.     Injury  to  cauda  equina  and  astasia-abasia  .         •         .  278 

45.  Dragging  of  the  foot  in  traumatic  hysteria          ......  282 

46.  Anesthesia  chart.     Traumatic  hysteria      .......  283 

47.  Field  of  vision.     Traumatic  hysteria .  284 

48.  Anaesthesia  chart.     Hemianaesthesia ........  293 

49.  Anaesthesia  chart.     Disseminated  anaesthesia     ......  293 

50.  Field  of  vision.     Concentric  contraction     .         .         .         .         .         .         .297 

51.  Footprints  in  hysterical  and  organic  hemiplegia         .....  303 

52.  Anaesthesia  chart.     Hysterical  paraplegia 306 

53.  Hysterical  contracture  at  wrist 309 

54.  Attitude  in  hysterical  coxalgia 314 

55.  Some  members  of  the  Freeman  family 360 


ACCIDENT   AND    INJURY. 


INTRODUCTION. 

THE   CONSIDERATION   OF   THE   CASE. 

No  sharp  line  of  demarcation  can  be  drawn  between  the 
disorders  of  the  nervous  system  which  develop  as  a  result 
of  acutely  occurring  injuries  and  those  which  owe  their 
existence  to  causes  operating  more  slowly,  or  whose  clinical 
manifestations,  although  they  may  appear  suddenly,  are  the 
effects  of  subtle  morbid  conditions  that  have  been  for  a 
long  time  active.  Yet,  as  every  causal  factor  adds  its  spe- 
cial cachet  to  the  conditions  it  induces,  so  injury  and  shock 
put  their  stamps  upon  the  nervous  affections  which  are 
their  results.  It  is  the  effects  of  traumatisms  upon  the  nerv- 
ous system  which  will  be  considered  in  the  following  pages. 
The  word  traumatic  is  permitted  so  many  meanings  that 
its  limitations  must  be  clearly  understood.  In  its  most  re- 
stricted sense  it  applies  only  to  such  injuries  as  are  the  re- 
sults of  acutely  acting  physical  violence,  while  in  its  widest 
meaning  it  includes  any  detriment  to  health  which  originates 
outside  of  the  body.  By  the  first  meaning  of  the  term 
psychic  influences  are  disregarded  ;  by  the  latter  interpreta- 
tion its  scope  would  be  practically  unlimited,  as  it  would 
include  all  morbid  conditions  which  owe  their  existence  to 
toxic  or  mechanical  causes,  such  as  lead  poisoning,  alcohol- 
ism, or  writer's  cramp,  as  well  as  the  crushing  of  nervous 
tissue  from  the  pressure  of  broken-down  protecting  struc- 


V  /.  , 


INTRODUCTION. 


ture,  or  the  disturbance  of  equilibrium  in  cerebral  processes 
brought  about  by  mental  shock  or  fright.  For  clinical  pur- 
poses neither  of  these  interpretations  of  the  term  is  satisfac- 
tory. The  first  disregards  the  very  important  influence  of 
nervous  shock  and  fright  as  disease-inducing  agents,  and 
the  second  renders  the  word  traumatic  much  more  compre- 
hensive than  is  desirable,  or  than  is  generally  understood. 
In  the  following  pages  traumatic  will  be  used  as  indicating 
quickly  acting  physical  violence  or  psychic  shock  which  arises  out- 
side the  body.  The  functional  traumatic  nervous  disorders 
have  received  careful  observation  and  description  by  neu- 
rologists ;  but  the  behavior  of  the  nervous  system  under 
injuries  which  directly  affect  nervous  structure  has  been 
too  little  subjected  to  special  investigation.  Most  acutely 
occurring  injuries  to  the  brain  and  spinal  cord  are  received 
in  surgical  wards,  where  the  exact  character  of  nervous 
symptoms  and  the  probable  location  of  lesions  only  occa- 
sionally become  the  objects  of  close  study.  Yet  organic 
injuries  to  the  nervous  system  constitute  a  field  of  investi- 
gation full  of  fruitful  promise.  There  are  constantly  occur- 
ring in  all  large  cities  selective  injuries  to  nervous  tissue, 
which  result  from  all  varieties  of  causes  and  which  occur 
under  all  possible  conditions.  Were  they  systematically 
examined  at  the  bedside,  and  were  the  clinical  picture,  when 
possible,  amplified  by  a  microscopic  study  of  the  patho- 
logical conditions  to  which  the  symptoms  had  been  due, 
these  injuries  could  be  made  to  subserve  the  purposes  of 
experimental  pathology,  and  could  be  relied  upon  to  furnish 
more  valuable  results  than  have  been  obtained  by  experi- 
ments on  animals. 

It  is  from  the  observations  of  morbid  conditions  as  they 
occur  in  man  that  we  must  look  for  the  answers  to  such 
questions  as  concussion  of  the  spinal  cord,  or  the  localiza- 
tion of  special  functions,  or  the  understanding  of  the  factors 
of  predisposition  to  nervous  disease,  or  the  indications  for 


THE   CONSIDERATION   OF   THE   CASE.  ^ 

operative  treatment.  That  the  subject  has  been,  and  still 
is,  treated  with  less  attention  than  it  deserves,  there  is,  un- 
fortunately, no  question  of  doubt.  Injuries  to  the  spinal 
cord  are  as  old  as  the  art  of  medicine  itself ;  yet  it  is  only 
within  the  last  decade  that  there  has  arisen  any  definite 
knowledge  as  to  the  localization  of  function  of  the  spinal- 
cord  segments.  Such  knowledge  as  we  now  possess  is 
largely  due  to  the  study  of  traumatic  cases. 

In  many  cases  of  traumatic  nervous  disease  the  clinical 
picture  is  so  plain  that  a  cursory  examination  suffices  for  an 
immediate  and  correct  appreciation  of  the  cause,  the  nature 
and  the  probable  outcome  of  the  injury.  The  ambulance 
surgeon  can  often  diagnosticate  a  fracture  of  the  spine  from 
the  seat  of  the  ambulance,  and  fractures  of  the  skull  are  of 
so  common  occurrence  in  emergency  hospitals  that  experi- 
enced surgeons  recognize  the  condition  by  the  general  ap- 
pearance of  the  patient  alone.  Yet  from  the  organic  lesions 
of  the  nervous  system,  whose  nature  is  readily  apparent,  to 
those  which  require  the  closest  study  and  rarest  skill  for 
their  diagnosis,  is  not  so  very  long  a  step.  In  presumable 
brain  injuries,  when  the  patient  is  comatose  or  delirious, 
examination  for  localizing  signs  is  often  unsatisfactory,  and 
the  history  of  the  accident  may  be  unobtainable,  or  if  told 
by  witnesses  unreliable,  so  that  the  diagnosis  of  fracture  of 
the  skull  or  laceration  of  the  brain,  as  opposed  to  some  of 
the  idiopathic  forms  of  coma,  is  very  difficult  or  at  times 
even  impossible. 

In  the  diagnosis  of  the  puzzling  forms  of  traumatism  of 
the  back — as  a  result  of  which,  without  evidences  of  lesion 
to  the  vertebras,  there  are  selective  symptoms  of  injury  to 
the  spinal  cord — considerable  knowledge  of  the  anatomy 
and  pathology  of  the  nervous  system  is  often  necessary. 
This  fact  becomes  evident  upon  the  perusal  of  the  works  of 
Erichsen,  the  pioneer  in  traumatic  neurology,  who  failed  to 
recognize  the  true  condition  in  many  cases  of  back  injury. 


4  INTRODUCTION. 

Affections  so  common  as  traumatic  peripheral  nerve  palsies, 
especially  those  which  affect  the  nerves  around  the  shoulder 
joint,  can  in  certain  cases  be  recognized  only  by  careful  elec- 
trical examination.  The  diagnosis  of  the  disorders  which 
must  still  be  known  as  functional  are  diagnoses  by  exclusion, 
to  make  which  presupposes  a  considerable  knowledge  of  the 
symptoms  of  organic  nervous  injuries. 

K  functional,  as  opposed  to  an  organic  disease  of  the  nerv- 
ous system,  is  one  in  which  the  anatomical  integrity  of  nerv- 
ous structure  remains  unimpaired.  There  may  be  serious 
or  even  alarming  symptoms,  yet  the  evidences  which  indi- 
cate destruction  of  special  centers  or  conducting  paths  are 
regularly  absent ;  also,  the  course  of  the  disease  is  benign, 
tending  to  recovery.  Although  there  is  no  reason  to  doubt 
that  every  departure  from  health  is  a  result  of  changes 
of  some  character  in  physical  structure  or  composition, 
the  morbid  alterations  in  nervous  tissue  which  underlie 
the  functional  nervous  diseases  have  hitherto  escaped  iden- 
tification, and  until  they  are  identified  these  affections  must 
be  classed  as  depending  upon  no  known  pathological  con- 
ditions. They  can  only  be  diagnosticated  as  functional, 
however,  when  careful  examination  has  demonstrated  that 
there  is  absence  of  those  symptoms  which  are  the  infal- 
lible signs  of  morbid  conditions  of  recognized  structural 
character. 

To  the  inherent  difficulties  of  diagnosis  which  are  due 
to  the  intricacies  of  the  anatomy  and  physiology  of  the 
nervous  system,  the  commercial  spirit  of  the  times  has 
added  others.  The  bringing  of  claims  for  damages  for  per- 
sonal injuries  has  reached  so  exaggerated  a  degree  that  it  is 
no  rare  occurrence  for  an  injured  person  to  see  an  attorney 
before  he  sees  a  doctor;  and  the  story  which  this  latter 
hears  often  speaks  more  eloquently  for  the  medical  knowl- 
edge of  certain  members  of  the  legal  profession  than  for  the 
veracity  of  the  patient. 


THE   CONSIDERATION   OF   THE   CASE.  c 

If  the  injuries  are  to  become  the  basis  for  a  claim  for 
damages,  there  are  many  complicating  factors.  Under 
these  circumstances,  while  the  account  of  the  resulting 
symptoms  is  to  be  listened  to  with  attention  and  respect,  it 
should  be  accepted  with  reserve,  and  only  in  so  far  as  it  may 
seem  to  be  justified  by  the  attendant  circumstances.  Such 
conservatism  can  not  be  construed  as  a  reflection  upon  the 
honesty  of  the  patient  or  of  his  lawyer.  As  a  rule  of  clini- 
cal medicine  it  is  universally  observed,  and  is  necessary  for 
the  avoidance  of  the  deception  caused  by  the  misstatements 
of  ignorance  as  well  as  those  of  intention.  The  question  of 
liability,  which  figures  very  prominently  in  many  cases,  is 
one  with  which  the  physician  has  little  to  do.  It  concerns 
him  only  in  so  far  as  he  may  be  able  to  show  that  the  physi- 
cal or  mental  condition  of  the  claimant  at  the  time  of  the 
accident  was  of  a  character  such  as  to  render  him  unable 
to  take  proper  precautions  against  danger. 

In  the  study  of  traumatic  nervous  disease  so  many 
factors  enter  that  it  has  seemed  more  advisable  to  en- 
title this  introductory  chapter,  which  essays  to  outline 
some  of  the  simpler  methods  of  investigation,  a  consid- 
eration of  the  case  rather  than  an  examination  of  the 
patient.  As  the  most  successful  physicians  are  those 
who  treat  patients  rather  than  diseases,  so  he  can  give 
the  most  valuable  opinion  in  regard  to  an  injury  of  the 
nervous  system  who  has  considered  it  from  every  point 
of  view. 

The  necessity  for  a  painstaking  examination  of  cases 
which  are  in  themselves  obscure,  or  for  those  in  which  for 
forensic  reasons  accuracy  of  diagnosis  is  especially  essen- 
tial, needs  no  emphasis.  It  is  always  advisable  to  put  the 
results  of  examination  immediately  in  writing,  and  in  med- 
ico-legal cases  it  is  well  to  have  the  assistance  of  a  stenog-. 
rapher,  in  order  that  the  procedure  may  not  be  unneces- 
sarily delayed  and  that  as  full  notes  as   possible    may    be 


6  INTRODUCTION. 

taken.     The   examination   may   best   be   divided   into   four 
stages,  viz. : 

I.  Previous  history  of  the  patient  (ancestral ;  personal). 

II.  History  of  the  accident. 

III.  Physical  evidences  of  predisposition  to  nervous  dis- 
ease. 

IV.  Examination  for  the  actual  injury. 

I.  Previous  History  of  the  Patient. 

In  nervous  disease  originating  as  the  result  of  injury 
the  influence  of  hereditary  predisposition  is  usually  not 
ver}^  evident,  and  is  always  difficult  to  prove.  Few  nerv- 
ous diseases  are  directly  transmitted  from  parent  to  child  ; 
heredity  seems  rather  to  act  by  giving  to  the  offspring 
a  nervous  system  whose  powers  of  resistance  are  dimin- 
ished, but  in  which  the  development  of  disease  depends 
upon  the  specific  action  of  various  exciting  causes  which 
vary  with  environment.  Among  the  morbid  conditions 
which  render  their  victims  particularly  prone  to  transmit 
unstable  nervous  systems  to  descendants  may  be  mentioned 
alcoholism,  insanity,  epilepsy,  syphilis,  hysteria,  and  tuber- 
culosis. If  any  of  them  have  been  present  in  both  parents^ 
or  have  been  generally  disseminated  throughout  a  family, 
the  chances  are  all  the  greater  that  the  offspring  will  be 
endowed  with  an  imperfectly  developed  nervous  system,  or 
with  one  which  will  easily  succumb  to  injurious  influences. 

The  object  sought  for  in  traumatic  cases  in  inquiring  for 
a  history  of  the  patient's  personal  life  is  to  establish  whether 
he  were  or  were  not  a  healthy  man  before  the  accident. 
The  patient  is  asked  the  diseases  he  has  had,  the  amount 
of  work  he  has  been  capable  of,  and  the  kind  of  life  he 
has  been  able  to  lead.  More  valuable  than  his  own  replies 
as  to  his  physical  condition  are  facts  concerning  his  sur- 
roundings and  mode  of  life.     Age,  sex,  nationality,  and  race 


HISTORY   OF   THE   ACCIDENT.  7 

are  considerations  of  paramount  importance,  which  are  de- 
scribed in  succeeding-  pages.  Certain  occupations,  notably 
those  which  expose  the  workman  to  chronic  poisonings,  are 
important  predisponents  to  nervous  disease.  On  account  of 
real  or  assumed  ignorance,  reliable  information  concerning- 
the  family  or  personal  history  is  often  difficult  to  obtain, 
and  the  physician  will  do  well  to  avoid  putting  too  much 
credence  in  statements  which  seem  at  variance  with  the 
actual  condition  of  the  patient. 

II.  History  of  the  Accident. 

Definite  and  reliable  information  concerning  the  accident 
is  often  unobtainable.  In  general  accidents,  such  as  railway 
collisions,  where  a  large  number  of  persons  are  involved, 
there  are  usually  no  spectators.  The  circumstances  which 
surround  such  catastrophes  make  each  individual  a  partici- 
pator rather  than  a  witness;  and  the  suddenness  of  the 
accident  and  the  terror  which  it  causes  usually  render  the 
victim  unable  to  give  an  intelligent  account  of  the  way  his 
own  injuries  were  received.  Even  if  he  were  not  rendered 
unconscious,  he  is  rarely  able  to  describe  just  what  befell 
him.  When,  however,  statements  are  obtainable  from  wit- 
nesses, such  testimony  is  often  more  valuable  than  that  of 
the  victim  himself. 

In  the  absence  of  information  as  to  the  exact  details  there 
is  usually  no  difficulty  in  learning  the  general  characters 
of  an  accident,  from  which  much  may  be  inferred  as  to 
its  probable  results.  The  law  of  averages,  or  the  *'  law 
of  the  long  run,"  as  Prof.  Mendenhall  (Science,  Decem- 
ber, 1895)  calls  it,  holds  good  here  as  elsewhere,  so  that 
each  variety  of  casualty  has  its  own  ratios  of  character- 
istic effects.  How  unvarying  these  effects  are,  when  de-. 
termined  by  sufficiently  extensive  observations,  is  shown 
by  the  following  tables,  which  have  been  kindly  furnished 


8 


INTRODUCTION. 


me  by  an  officer  of  one  of  the  largest  railway  systems  of 
America. 

They  relate  to  accidents  and  injuries  of  all  characters 
which  have  occurred  in  the  past  six  years  on  or  about  the 
railway  or  in  any  of  the  shops  of  the  company.  They  have 
proved  to  be  of  invaluable  service  to  the  public,  to  em- 
ployees, and  to  the  railway  company,  for,  by  showing  the 
varieties  of  accident  which  are  most  frequent  and  the  con- 
ditions under  which  they  are  most  liable  to  occur,  they  call 
official  attention  to  faults  in  construction  or  operation,  and 
thus  furnish  the  surest  means  of  diminishing  the  chances  of 
personal  injury. 

Lack  of  space  prevents  me  from  reproducing  all  the 
ratios  which  this  able  statistician  has  generously  placed  at 
my  disposal.  The  three  following  tables,  however,  illus- 
trate the  general  character  of  his  work  and  the  inferences 
which  may  be  drawn  from  it : 


Table  i. 
Injuries  to  Passengers. 


Year. 


Where,  etc.  : 

On  passenger  trains 

On  freight  trains 

On  station  grounds,  etc 

Postal  and  expressmen 

Cause  : 

Collisions 

Getting  on  and  off  moving  trains . . 

Getting  on  and  off  trains  after  stop 
made 

Defective  and  unlighted  stations  and 
platforms 

Miscellaneous 

Result  : 

Death 

Loss  of  limb 

Loss  of  finger  or  toe 

Spinal  injury i 

Fracture  or  dislocation 

Sprain 

Cuts  and  bruises 

Miscellaneous 


87.5 
8.2 

4-3 
14.0 

27.6 
17.2 

3-5 

0.8 
50.9 

5-0 
1-5 
1-5 
4-7 
8.6 

3-9 
48.3 
26.5 


88.9 

2.5 
8.6 
5-0 

42.7 
10.3 


0.2 
44.4 


2.2 

3-5 

5-7 

63.2 

15-3 


83.1 
3-8 

I3-I 
6.1 

16.9 
27.9 

7-9 


47-3 

10.8 
1.6 

2-3 

II. 6 

6.6 

34-3 
32.8 


80.6 
8.6 

10.8 
2.1 

8.0 
28.0 

10.8 

2.1 

1.4 

1.4 

0.7 

0.7 

8.6 

.6.4 

55-0 

25.8 


79.1 

5-3 

15-6 

4.2 

8.0 
14-5 

8.6 

2.2 

56.7 

9-5 
0.6 

1.2 

8.7 

12.3 

44-7 
23.0 


HISTORY   OF    THE   ACCIDENT. 


Table  2. 

Injuries  to  Employees. 


Employment  : 

Conductors 

Enginemen 

Firemen 

Brakemen 

Mechanics 

Warehousemen 

Laborers 

Miscellaneous 

Cause  : 

Coupling 

Collisions 

Getting  on  and  off  trains 

Caught  in  frogs  and  switches  . 

Use  of  tools  and  machinery.. . 

Fell  from  cars 

Defective  tools  and  appliances 

Miscellaneous 

Result  : 

Death 

Loss  of  limb 

Loss  of  finger  or  toe 

Spinal  injury 

Fracture  or  dislocation 

Sprain 

Cuts  and  bruises 

Miscellaneous 


i8gi. 

1892. 

1893. 

1894. 

189s. 

5-3 

6.4 

7.2 

7.8 

5-0 

2.0 

2.6 

2.9 

2.2 

2.6 

4.2 

3-5 

5-0 

4.4 

4.1 

45.1 

45-8 

44-3 

39-1 

30.8 

18.4 

16.2 

18.8 

19.4 

28.0 

I.O 

0.7 

0.7 

0.4 

0.4 

16.0 

16.6 

13.8 

10.8 

15.8 

8.0 

8.2 

7-3 

15.9 

13-3 

28.6 

27.9 

26.3 

23-2 

17.4 

1.9 

2.4 

3-8 

2.5 

2.2 

7-3 

7.2 

6.5 

8.0 

7.0 

0.2 

0.1 

0.1 

0.3 

0.1 

7.8 

0.6 

3-2 

13.8 

22.3 

5.5 

4.8 

4.9 

5.6 

4-3 

1.8 

0.6 

1.2 

0.5 

0.6 

49-7 

56-4 

55-2 

46.1 

46.1 

3-9 

4.0 

3-0 

2.5 

1-3 

1.4 

I.I 

I.I 

1.2 

0.4 

3-2 

3-4 

3-4 

3-3 

2.3 

0.1 

1-3 

2.7 

0.6 

0.1 

6.2 

6-3 

6.0 

5-3 

4.9 

14. 1 

13.0 

II. 0 

16.3 

15-2 

47.7 

50.0 

49.6 

39-4 

50.1 

23-4 

20.9 

23.2 

31.4 

25-7 

4.8 

2.1 

4-3 
26.0 
34-6 

0.8 
16.7 
10.7 

II. I 
1-3 
7-5 
0.4 

28.0 
4.1 
1.6 

47.6 


Table  3, 
Percentage  of  Results. 


Year. 


1893. 


1895. 


Result  : 

Death 

Loss  of  limb 

Loss  of  finger  or  toe..  . 

Spinal  injury 

Fracture  or  dislocation, 

Sprain 

Cuts  and  bruises 

Miscellaneous 

Total : 

Passengers 

Travelers  on  highway. . 

Employees 

Trespassers 

Total 


10.3 

2.7 

3-0 

0.4 

6.6 

10.9 

44.9 

21.2 

257 

190 

2,488 

455 


9.0 

2.2 

3-0 

1-3 

6.6 

10.5 

47.2 

20.2 

221 

239 

3>io5 

492 


8.5 
2.1 
2.7 

2.7 
6.6 
9.1 

47-4 
20.9 

281 

179 

3.087 

447 


8.6 

2.3 

2.6 

0.6 

6.2 

13-5 

36.6 

29.6 

130 

195 

2,339 

430 


6.1 
1.4 

2.0 
0.2 

5-7 
13-3 
46.5 

24.8 

139 
196 

3,854 
^433 


5-9 
1.0 

1-3 

0.2 
4.8 

15-3 
48.8 
22.7 

187 

184 

3.753- 

399 


3.390 


4.057 


3.994 


3,094 


4,622 


4.523 


lO  INTRODUCTION. 

All  these  statistics  are  self-explanatory.  The  first  "and 
second  tables  show  the  distribution  of  accidents  among-  pas- 
sengers and  employees  respectively ;  table  3  shows  the  per- 
centage results  of  all  accidents  and  the  total  number  of 
injured  persons  upon  which  the  statistics  are  based. 

From  the  study  of  these  tables  it  appears  that  the  larger 
number  of  these  casualties  are  trivial  and  occur  among  em- 
ployees, and  are  consequently  unattended  with  medico-legal 
questions,  so  that  the  percentage  of  injuries  to  the  nervous 
system  is  very  much  less  than  one  would  suppose  by  read- 
ing court  records. 

What  is  true  for  railway  accidents  is  also  true  for  other 
kinds  of  casualties — namely,  that  their  character  determines, 
to  a  certain  extent,  the  nature  of  the  resulting  injuries.  In 
the  consideration  of  individual  cases  it  is,  of  course,  impossi- 
ble to  rely  too  largely  on  generalizations.  Although  it  may 
be  known  that  certain  causes  are  usually  followed  by  similar 
results,  a  variation  of  conditions  may  bring  about  excep- 
tions. In  most  cases,  however,  the  character  of  the  accident 
is  an  index  of  the  severity  and  the  nature  of  the  resulting 
injuries.  In  serious  general  accidents  the  body  may  be 
subjected  to  every  degree  of  violence,  which  may  induce 
immediate  death  or  cause  mutilations  of  all  degrees.  The 
fate  of  passengers  or  employees  in  any  single  given  collision 
or  derailment  can  not,  of  course,  be  foretold.  On  the  other 
hand,  it  can  be  positively  stated  that  the  sudden  stopping  or 
starting  of  a  vehicle,  by  which  the  passenger  may  be  jarred 
but  receives  no  external  wound,  rarely  if  ever  exerts  suffi- 
cient force  to  cause  irreparable  injury  to  the  nervous  system. 
In  many  other  forms  of  mishap  we  are  justified  in  inferring 
that  the  violence  was  inadequate  to  cause  structural  injury. 
Thus,  a  light  pasteboard  box  falls  a  few  feet  and  strikes  a 
young  girl  on  the  head  without  inflicting  any  serious  wound. 
She  immediately  goes  into  convulsions,  and,  on  regaining 
consciousness,  it  is  found  that  she  is  insensible  on  the  left  side 


PHYSICAL   EVIDENCES.  II 

of  the  body.  In  such  a  case  it  is  just  to  infer  at  once  that  the 
injury  could  not  have  caused  any  lesion  of  the  brain  which 
might  explain  the  symptoms,  but  rather  that  they  were  due 
to  the  disordered  mental  state  of  the  patient,  and  were  the 
immediate  results  of  fright. 

III.  Physical  Evidences  of  Predisposition  to 
Nervous  Disease. 

In  severe  injuries,  such  as  fractures  of  the  skull  or  of 
the  vertebrae,  the  previous  condition  of  the  patient  is  of 
secondary  importance.  A  strong  man  may  of  course  sur- 
vive a  shock  that  might  prove  fatal  to  the  patient  whose 
recuperative  powers  had  been  enfeebled  through  previous 
bad  health  or  excess.  Yet  such  a  difference  can  rarely  be 
positively  proved.  The  chief  forensic  importance  of  previ- 
ous condition  attaches  to  those  disorders  of  which  the  excit- 
ing cause  has  not  been  immediately  dangerous  to  life,  but 
has  been  the  alleged  starting  point  of  diseases  which  are 
more  or  less  serious  though  not  directly  fatal.  The  possi- 
bility of  error  in  ascribing  a  traumatic  origin  to  a  disease 
which  antedated  the  injury  is  considered  in  Part  III.  Here 
it  is  necessary  to  mention  only  such  conditions  as  furnish  a 
favorable  soil  for  the  development  of  nervous  affections. 
There  are  certain  anatomical  evidences  which  are  regarded 
as  indicative  of  a  congenitally  defective  nervous  system 
which  is  consequently  less  tolerant  of  injurious  influences. 
These  are  the  stig7nata  of  degeneration,  and,  although  it 
would  be  beyond  the  scope  of  these  pages  to  describe  them 
in  detail,  their  general  character  may  be  seen  in  the  fol- 
lowing classification  as  suggested  by  Peterson  :  * 

*  State  Hospitals  Bulletin,  July,  1896. 


12 


INTRODUCTION. 


Stigmata  of  Degeneration. 


^       .  ,  ,.        i  Asymmetry. 

Cranial  anomalies,  i  ^^  . 

(  Deformities. 


Facial  asymmetry. 


Prognathism. 
Retrognathism. 
Deformities  of  the  palate. 
Dental  anomalies. 

j  Harelip  and  cleft   palate  not 
(      certainly  stigmata. 


Anomalies  of  the  tongue  and  lips. 
Anomalies  of  the  nose. 


Anomalies  of  the  eye.       < 


Anomalies  of  the  ear. 


Flecks  on  the  iris,  strabismus,  chromatic 
asymmetry  of  the  iris,  narrow  palpe- 
bral fissures. 

Albinism. 

Congenital  cataracts. 

Microphthalmos. 

Pigmentary  retinitis. 

Muscular  insufficiency. 


Anomalies  of  the  limbs.   < 


'  Polydactyly. 

Syndactyly. 

Ectrodactyly. 

Symelus. 

Ectromelus. 

Phocomelus. 
^  Excessive  length  of  the  arms. 

Hernias. 

Malformation  of  the  breasts,  thorax. 

Dwarfishness. 

Giantism. 

Infantilism. 

Feminism. 

Masculinism. 
.  Spina  bifida. 
'  Cryptorchismus. 

Microrchidia. 
Anomalies  of  the  genital   ,  Spurious  hermaphroditism. 

Hypospadia. 

Epispadia. 

Atresia. 


Anomalies  of  the  body 
in  general. 


organs. 


PHYSICAL    EVIDENCES. 


13 


r  Polysarcia. 

.    ,       ,  .  Hypertrichosis. 

Anomalies  of  the  skin.     <    ./  .r    • 

Absence  of  hair. 

I  Premature  grayness. 

The  practical  value  of  the  stigmata  of  degeneration  is 
impaired  by  the  fact  that  they  occur  chiefly  in  idiots,  luna- 
tics, and  epileptics,  about  whose  degeneracy  there  could  be 
no  question.  Also,  almost  any  one  of  them  may  occur  in 
persons  who  never  present  any  other  structural  or  functional 
anomalies. 

More  useful  from  a  diagnostic  point  of  view  than  these 
physical  telltales  of  ancestral  faults  are  such  evidences  of 
acquired  predisposition  as  are  left  by  certain  diseases  and 
by  certain  poisons.  In  a  general  way  it  may  be  said  that 
any  disease  which  impairs  the  general  health  makes  the  de- 
velopment of  nervous  disorders  more  probable.  There  are 
a  few  conditions,  however,  which  stand  so  pre-eminently  in 
a  causal  relation  to  neural  diseases  that  it  is  very  necessary 
to  determine  their  existence  before  attributing  too  high  a 
value  to  any  exciting  cause.  Of  these,  the  most  important 
are  alcoholism,  syphilis,  and  arterio-sclerosis. 

Alcoholism. — It  is  a  matter  of  common  remark  that 
drunken  persons  who  are  in  serious  accidents  often  escape 
without  any  severe  injury,  or  indeed  any  subsequent  ill- 
effects  whatsoever.  While  it  can  not  be  denied  that  the  mus- 
cular relaxation  and  mental  stupor  of  alcoholic  intoxication 
not  infrequently  furnish  a  means  of  escape  from  physical 
injury  and  psychic  shock,  this  is  a  very  minor  considera- 
tion when  compared  with  the  number  of  persons  who  are 
killed  or  injured  in  accidents  which  would  not  have  occurred 
to  an  individual  who  was  sober.  Alcoholism  stands  in  a 
very  important  causal  relation  to  traumatic  diseases  of  all 
kinds,  but  especially  to  traumatic  diseases  of  the  nervous 
system.  It  is  frequently  accountable  for  the  accident  and 
the  injury,  and  always  is   prejudicial  to  recovery.      After 


14 


INTRODUCTION. 


very  slight  blows  on  the  head,  or  after  trivial  injuries  to 
other  parts  of  the  body,  alcoholic  persons  not  uncommonly 
develop  delirium  tremens,  pneumonia,  or  heart  failure,  or 
show  in  other  ways  that  their  recuperative  powers  have 
become  impaired  by-  alcohol.  The  evils  of  the  drinking 
habit  are  so  widely  disseminated  in  all  classes  of  society 
that  it  is  very  essential  at  the  beginning  of  an  examination 
of  any  accident  case  to  determine  the  presence  or  absence 
of  chronic  alcoholic  poisoning  as  a  complicating  factor. 
Old  and  steady  drinkers  present  at  all  times  such  unmistak- 
able physical  stigmata  of  their  vice  that  there  is  no  difficulty 
in  doing  this.  But  man}-  persons  who  have  regarded  them- 
selves as  moderate  drinkers  only,  and  who  present  none  of 
the  more  evident  signs  of  chronic  alcoholic  poisoning,  after 
slight  injuries,  exhibit  symptoms  which  show  that  their  use 
of  alcohol  has  been  too  free.  In  such  cases  the  historj'  of 
excessive  drinking  is  not  necessar\^  for  its  diagnosis,  because 
there  is  so  great  a  variation  in  the  individual  tolerance  to 
the  poison  that  a  daily  quantity  which  in  one  person  could 
be  taken  without  evil  effects  of  any  kind  might  be  sufficient 
in  some  one  else  to  cause  acute  symptoms,  or  to  render  the 
organism  incapable  of  overcoming  visitations,  such  as  a 
health}-  man  could  easily  resist.  Accordingly,  more  reli- 
ance is  to  be  placed  upon  those  evidences  of  alcoholism 
which  the  physician  may  discover,  rather  than  upon  the 
patient's  history.  They  are  usually  abundantly  and  charac- 
teristically present,  and  are  both  physical  and  mental. 

The  physical  symptoms  consist  of  tremor,  generalized 
or  most  prominent  in  the  face,  lips  and  tongue,  and  in  the 
fingers  ;  the  skin  may  be  normal,  or  may  be  flabby  and  pale, 
with  a  peculiar  appearance  of  oedema ;  gastric  irritability  is 
common;  the  heart  is  usually  rapid,  and  there  may  be  an 
impairment  of  the  purity  of  the  first  sound  at  the  apex ; 
the  functions  of  the  special  senses  are  often  vitiated,  and 
disturbances  of  general  cutaneous  sensation,  both  objective 


PHYSICAL   EVIDENCES. 


15 


and  subjective,  are  particularly  frequent.  The  mental  S3'mp- 
toms  consist  of  coma  or  stupor  or  delirium  and  their  vari- 
ations. The  delirium  is  usually  characterized  by  hallucina- 
tions of  sight,  less  frequently  of  the  other  senses,  which 
almost  always  have  reference  to  living  objects,  such  as  ani- 
mals or  crawling  things  or  strange  persons.  A  common 
condition  is  one  of  forgetfulness  and  confusion ;  the  memory 
may  be  lost  for  considerable  periods  of  time,  or  the  patient 
may  be  unable  to  collect  himself  sufficiently  to  tell  where  he 
is  or  how  he  came  there.  Two  patients  whom  I  recently 
saw  at  the  Manhattan  Hospital  thought  they  went  out  every 
night,  when  in  reality  they  both  had  been  in  bed  for  several 
weeks.  Systematized  delusions  are  not  common,  although 
they  sometimes  occur  in  the  chronic  form  of  poisoning,  and 
consist  with  particular  frequency  of  false  beliefs  in  regard 
to  marital  infidelity. 

The  fact  that  the  symptoms  of  chronic  alcoholic  poisoning 
resemble  in  many  respects  those  of  Oppenheim's  "traumatic 
neurosis  "  has  led  Saenger*  to  suggest  the  possibility  that 
many  of  those  cases  are  in  reality  cases  of  chronic  alcohol- 
ism which  have  been  made  worse  by  injury.  The  tremor, 
amblyopia,  impairment  of  cutaneous  sensibility,  and  rapid 
pulse,  which  are  prominent  in  the  "  traumatic  neurosis,"  are 
all  found  in  ethylism.  Whether  some  of  these  cases  are  in 
reality  nothing  but  "  traumatic  alcoholism,"  or  whether  the 
chronic  toxsemia  has  supplied  the  foundation  upon  which 
has  developed  a  neurosis  or  psychosis,  we  are  at  present 
unable  to  decide  definitely.  It  is  certain,  however,  that 
in  many  of  the  cases  which  will  be  described  later  alco- 
holism has  played  a  very  important  role. 

Syphilis. — The  typical  history  of  syphilis  is  obtainable  in 
a  certain  number  of  the  cases  of  nervous  disease.  In  a 
large  number  there  is  the  admission  of  a  sore  on  the  penis 

*  Die  Beurtheilung  der  Nervenerkrankungen  nach  Unfall,  Stuttgart,  1S96. 


1 6  INTRODUCTION, 

only,  but  of  no  subsequent  syphilitic  manifestations ;  in 
many  instances  the  patients  deny  every  symptom  which 
might  have  been  of  specific  character.  In  the  absence  of 
a  syphilitic  history,  there  are  often  discoverable  certain 
physical  defects  which  indicate  that  the  syphilitic  poison 
had  at  one  time  been  active.  Of  these  the  most  important 
are  scars  on  the  penis,  scars  on  the  legs,  adhesions  of  the 
iris,  and  similar  results  of  syphilitic  inflammation.  While 
these  evidences  are  oftentimes  characteristic,  it  is  rarely 
possible  to  assert  that  they  are  the  results  of  syphilis  and 
could  be  the  results  of  nothing  else,  although  in  the  clinic 
they  are  accepted,  usually  correctly,  as  satisfactory  evi- 
dences of  preceding  infection.  But  any  one  of  them  could 
owe  their  existence  to  other  causes,  and  it  is  consequently 
almost  impossible  to  be  certain  that  syphilis  has  existed 
when  all  active  syphilitic  processes  have  subsided. 

The  part  played  by  syphilis  in  the  aetiology  of  nervous 
disease  is  of  great  importance.  The  venereal  disease  has 
an  unquestioned  and  intimate  connection  with  the  causa- 
tion of  general  paresis  and  of  locomotor  ataxia.  After 
acute  injuries  to  the  nervous  system,  latent  syphilitic  pro- 
cesses not  uncommonly  become  active  and  give  the  symp- 
toms of  focal  lesions.  Syphilis,  like  alcoholism,  is  an  active 
factor  in  the  induction  of  premature  senility.  By  attacking 
the  blood-vessels  it  causes  serious  disturbances  of  the  circu- 
lation, which  lead  to  degenerative  changes  in  various  organs, 
and  which  render  the  organism  less  resistant  to  deleterious 
influences. 

It  is  also  a  significant  faictor  in  the  genesis  of  such  func- 
tional disorders  as  neurasthenia,  hysteria,  neuralgia,  and 
epilepsy. 

Arterio-sclerosis. — The  importance  of  the  relationship 
between  disease  of  the  arteries  and  certain  symptoms  of 
disturbances  of  nervous  function  can  hardly  be  overesti- 
mated.    By  attacking  the  coronary  arteries,  arterio-sclerosis 


PHYSICAL   EVIDENCES.  I7 

causes  a  degeneration  in  the  muscular  mechanism  of  the 
heart  with  a  consequent  deficiency  of  propulsive  power  in 
that  organ ;  by  diminishing  the  caliber  of  terminal  arteries, 
it  also  offers  serious  impediments  to  circulation.  The  pro- 
cess, in  whichever  way  it  acts,  is  a  direct  obstacle  to  blood 
supply  and  a  menace  to  nutrition.  Its  effects  are  wide- 
spread, but  particularly  disastrous  to  the  nervous  system. 
It  is  a  well-known  fact  that  arterial  degeneration  is  a  com- 
mon accompaniment  of  the  retrogressive  periods  of  life,  but 
it  is  too  little  recognized  that  it  is  not  rare  in  youth  and 
middle  age.  In  young  subjects  especially  the  effects  of 
alcohol  and  syphilis  are  prominent  in  its  causation.  In  the 
autopsies  on  the  bodies  of  prisoners  who  die  in  the  Work- 
house on  Blackwell's  Island,  arterio-sclerosis,  either  gener- 
alized or  chiefly  restricted  to  the  cerebral  arteries,  is  fre- 
quently encountered  in  subjects  who  are  under  forty  years 
of  age,  but  who  have  led  a  life  of  exposure  and  excess. 

Arterial  degeneration,  either  disseminated  or  limited  to 
the  cerebral  arteries,  may  exist  for  a  long  time  without 
causing  any  subjective  symptoms,  or  it  may  be  the  direct 
cause  of  dizziness,  failure  of  mental  power,  headache,  epi- 
leptiform attacks,  etc.  When  existent  it  is  directly  unfa- 
vorable to  recovery  from  acute  injuries,  both  by  reason  of 
its  causing  a  diminution  in  recuperative  power  and  because 
the  patients  are  particularly  liable  to  such  complications 
as  pneumonia  and  heart  weakness.  On  both  clinical  and 
pathological  grounds  it  is  probable  that  the  disturbances 
of  cerebral  circulation  which  it  causes  are  often  respon- 
sible for  many  nervous  symptoms  which  are  classed  as  func- 
tional. 

In  the  examination  of  an  accident  case,  accordingly,  it  is 
very  essential  to  determine  whether  the  injury  has  acted 
upon  a  perfectly  healthy  person  or  upon  one  whose  arteries 
were  diseased.  This  is  not  always  easy  to  do.  In  advanced 
stages   when   there  are  objective  signs,  such  as   thickened 


1 8  INTRODUCTION. 

peripheral  arteries,  a  hypertrophied  and  overacting-  heart 
whose  second  aortic  sound  is  intensified,  urine  with  low  spe- 
cific gravity  and  which  is,  perhaps,  slightly  albuminous,  the 
diagnosis  is  plain.  But  in  the  earlier  stages  one  or  all  ot 
these  signs  may  be  absent,  and,  although  the  previous  life  of 
the  patient  may  have  been  such  as  to  have  caused  degenera- 
tive vascular  changes,  there  are  no  objective  evidences  that 
such  conditions  exist.  Even  in  the  absence  of  objective 
signs  the  physician  should  hesitate  in  attributing  a  purely 
functional  character  to  such  symptoms  as  dizziness  or 
cardiac  irregularity  in  persons  whose  previous  life  has 
been  of  a  character  to  bring  about  degeneration  in  the 
circulatory  organs. 

IV.  The  Examination  for  the  Actual  Injury. 

In  addition  to  the  search  for  nervous  symptoms,  it  would 
seem  superfluous  to  emphasize  the  necessity  for  a  thorough 
general  physical  examination  of  the  patient  were  it  not  for 
the  fact  that  it  becomes  so  frequently  apparent,  in  both  clin- 
ical and  medico-legal  cases,  that  the  examination  has  been 
entirely  too  superficial  to  furnish  sufficient  grounds  for  a 
definite  opinion.  In  cases  of  organic  injury,  although  the 
nature  of  the  case  may  be  plain  at  the  first  glance,  the  more 
searchingly  the  physician  pushes  his  inquiries  the  more 
capable  will  he  be  of  giving  an  opinion  of  value.  In  func- 
tional nervous  disease  the  diagnosis  can  only  be  made  where 
it  can  be  proved  that  organic  disease  is  in  all  probability 
absent.  How  serious  may  be  the  errors  incurred  through 
superficiality  of  examination  was  illustrated  by  a  case  to 
which  my  attention  has  recently  been  called  : 

A  woman  sought  advice  for  a  peculiar  nervous  condition  which 
ensued  immediately  after  a  blow  on  the  head  from  a  heavy  bale 
of  carpets.  She  asserted  that  previously  to  this  she  had  been 
healthy  in  every  respect,  but  that  since  the  accident  she  had  been 
nervous,  emotional,  and   unable  to  concentrate  her  mind  on  her 


THE   EXAMINATION   FOR   THE   ACTUAL   INJURY.  jg 

work.  Immediately  after  the  accident  she  developed  huskiness 
of  speech  and  an  annoying  tracheal  cough,  very  similar  to  hysterical 
cough,  without  any  expectoration.  The  patient  was  extremely 
suggestible,  and  an  attempt  at  hypnotizing  her  was  successful  in 
inducing  the  first  degree  of  hypnosis.  The  condition  was  diag- 
nosticated by  the  physician  as  one  of  "  traumatic  neurosis."  A 
subsequent  examination  of  the  chest  and  larynx,  when  the  patient 
was  admitted  to  the  hospital,  revealed  unequivocal  evidences  of 
an  aneurism  of  the  aorta.  Thus,  although  the  nervous  symptoms 
were  undoubtedly  functional,  the  cough  and  laryngeal  symptoms 
were  the  expressions  of  a  fatal  disease  whose  existence  had  been 
entirely  overlooked. 

The  intimate  structural  and  functional  relationship  of  the 
nervous  system  to  every  organ  in  the  body,  and  the  fre- 
quent association  of  nervous  disease  with  diseases  of  other 
organs  or  systems,  render  any  examination  of  the  nervous 
system  incomplete  which  has  not  been  preceded  by  an 
investigation  of  general  somatic  conditions.  Such  a  pro- 
cedure is  always  essential  for  purposes  of  prognosis,  and  in 
many  cases  is  the  one  means  of  avoiding  diagnostic  errors. 
To  determine  the  presence  of  eruptions  or  cicatrices  or 
other  evidences  of  present  or  past  lesions  of  the  skin,  exami- 
nation of  the  whole  cutaneous  surface  is  often  necessary  ;  no 
examination  is  satisfactory  which  leaves  undetermined  the 
condition  of  the  heart  and  lungs ;  the  urine  must  be  tested 
for  the  presence  of  albumen  or  sugar — in  fact,  most  of  the 
important  means  of  diagnosis  must  be  resorted  to  before  the 
physician  can  hope  to  obtain  a  clear  comprehension  of  the 
case.  It  may  seem  almost  elementary  to  lay  stress  upon 
such  self-evident  facts,  but  it  is  certain  that  the  errors 
which  are  occasionally  laid  to  the  neurologist's  door  most 
frequently  arise  from  the  lack  of  thoroughness  in  this  re- 
spect. 

In  some  cases,  and  especially  if  the  patients  are  women, 
it  is  impossible  to  obtain  consent  to  a  complete  examination. 
Under  such  circumstances  the  physician  in  his  report  should 


20  INTRODUCTION. 

not  fail  to  mention  such  limitations,  and  should  only  give  a 
conditional  opinion. 

It  is  impossible  to  devise  any  scheme  of  examination 
which  is  in  every  way  satisfactory,  but  I  have  found  the 
following,  slightly  modified  from  Striimpell's,  the  most 
useful : 

General  appearance  (facial  expression,  manner,  etc.). 
Mental  state. 
Olfactory  nerve. 

Eyes — 2d,  3d,  4th,  and  6th  nerves. 
5th. 
7th. 
8th. 
9th. 

nerves  which  include  speech,  deglutition,  secre- 
tion of  saliva,  and  taste. 


O 


loth. 
nth. 
I2th. , 

Paralysis,  rigidity,  tremor,  morbid  movements,  gait. 

Sensation  (pain,  touch,  temperature,  muscular  sense). 

Reflex  action  (superficial  and  tendon  reflexes). 

Trophic  disturbances. 

Electrical  examination. 

General  Appearance. — In  many  cases  the  general  man- 
ner, the  facial  expression,  the  speech,  the  attitudes,  the  gait, 
point  at  once  to  the  condition  from  which  the  patient  is 
suffering,  and  indicate  the  special  functions  which  should 
receive  the  most  careful  investigation.  Many  nervous  dis- 
eases have  characteristic  physiognomies,  and  cause  pathog- 
nomonic movements.  From  the  manner  and  facial  expres- 
sion alone  it  is  often  possible  to  decide  as  to  the  existence 
of  real  or  supposed  pain,  of  insomnia,  or,  indeed,  if  the  pa- 
tient is  seriously  ill.  The  observation  of  the  face  in  certain 
diseases  (bulbar  palsy,  paralysis  agitans,  general  paresis)  is 
often  of  itself  sufficient  for  diagnosis.  Such  indications  are 
always  of  value  as   clinical  guides,  and   may  prove  to  be 


THE    EXAMINATION    FOR    THE   ACTUAL   INJURY.  2 1 

important  supports  of  the  final  diagnosis;  but  too  much 
weight  should  not  be  assigned  to  them  until  their  signifi- 
cance has  been  verified  by  the  results  of  more  extended 
examination. 

Mental  State. — After  organic  injury  to  the  spinal  cord  or 
peripheral  nerves  there  are  no  characteristic  mental  symp- 
toms unless  the  brain  is  injured  as  well.  The  mental  states 
in  hysteria  and  neurasthenia  will  be  described  with  those 
diseases. 

After  severe  head  injuries  the  patient  may  be  in  coma 
■or  be  stupid  and  delirious,  and  no  further  evidences  of  the 
mental  state  are  obtainable.  If,  after  slight  injuries,  there 
is  decided  impairment  or  perversion  of  the  mental  faculties, 
there  is  reason  to  suspect  that  some  disease  or  poisoning 
-affecting  the  mind  had  pre-existed.  Eccentricities  of  man- 
ner, carelessness  or  peculiarities  of  dress,  and  in  many  con- 
ditions the  facial  expression,  are  to  be  regarded  as  evi- 
•dences  of  mental  states. 

In  accident  cases  the  condition  of  the  memory  is,  for 
many  reasons,  of  special  importance.  It  should  be  ascer- 
tained how  much  the  patient  remembers  about  the  accident, 
-and  whether  he  is  cognizant  of  events  which  occurTed  just 
before  it,  or  during  it,  or  just  after  it.  If  he  were  rendered 
unconscious,  it  should  be  determined  how  soon  conscious- 
ness returned  and  memory  became  re-established.  The 
memory  for  recent  events  should  be  compared  with  mem- 
ory for  things  of  the  more  remote  past.  The  presence  or 
absence  of  systematized  amnesia  should  also  be  established. 
Next  to  memory,  the  power  of  fixing  the  attention  is  one  of 
the  most  important  of  mental  symptoms.  In  coma  and  deli- 
rium it  is  of  course  abolished  ;  but  often,  when  the  patient  is 
apparently  conscious,  he  shows  b}^  inattention  or  by  confu- 
sion that  he  has  very  little  idea  of  his  surroundings.  Delu- 
-sions,  illusions,  and  hallucinations  may  be  elicited  by  the 
physician  himself,  or  may  be  observed  by  attendants. 


2? 


INTRODUCTION. 


The  ability  to  read,  to  write,  to  comprehend,  or  to  re- 
peat written  or  spoken  words,  to  recognize  objects  by  any 
of  the  special  senses,  gives  important  information  in  regard 
to  aphasia,  or  psychical  speech  disturbances.  Dysarthria,  or 
interference  with  speech  through  physical  causes,  becomes 
apparent  upon  examination  of  the  cranial  nerves. 

The  Cranial  Nerves. 

Smell. — Olfactory  Nerve.^ — ^The  sense  of  smell  is  im- 
paired or  lost  in  injuries  to  the  olfactory  nerves  and  in 
hysteria.  It  should  be  remembered,  also,  that  it  may  be 
diminished  in  diseases  of  the  nose.  In  testing  for  it  one 
nostril  should  be  taken  at  a  time,  and  the  other  nostril 
tightly  closed. 

The  substances  ordinarily  used  are  musk,  peppermint,, 
asafoetida,  and  acids.  They  should  be  in  solution,  and  kept 
in  bottles  with  rubber  corks. 

The  Eyes. — Although  examination  of  the  eyes  includes 
the  examination  of  several  nerves,  they  may  be  most  con- 
veniently considered  together.  In  all  doubtful  cases,  test- 
ing of  the  various  ocular  functions  should  be  intrusted  to 
some  one  especially  familiar  with  them.  Every  physician^ 
however,  ought  to  be  able  to  examine  for  and  understand 
the  evidences  of  prominent  ocular  symptoms,  and  should  be 
able  to  use  both  the  ophthalmoscope  and  the  perimeter. 

The  first  step  in  the  examination  of  the  eyes  is  to  notice 
the  size  of  the  palpebral  fissure  and  the  prominence  of  the 
eyeball.  The  condition  of  the  upper  lid  as  to  elevation  or 
drooping  (ptosis),  the  ability  to  close  or  to  open  the  eye, 
renders  important  information  regarding,  respectivel)^  the 
seventh  and  third  nerves.  The  pupils  should  be  examined 
for  actual  and  comparative  size  one  to  the  other,  and  for 
irregularities  of  outline,  such  as  may  have  been  caused  by 
preceding  iritis.  The  contraction  of  the  pupil  under  the 
influence  of  light  is  usually  tested  either  by  covering  the  eye 


THE   CRANIAL   NERVES. 


23 


and  then  observing,  when  it  is  uncovered,  if  the  pupil  grows 
smaller,  or,  if  the  iris  is  very  dark,  the  converse  of  this 
procedure  is  often  easier — i.  e.,  after  the  eye  has  been  ex- 
posed to  light,  it  is  covered  with  a  dark  object,  and  it  is 
then  observed  if  it  dilates  in  the  shadow.  The  power  of 
accommodation  is  determined  by  having  the  patient  alter- 
nately look  at  a  near  object  and  then  at  a  distant  one,  and 
observing  the  change  in  the  pupillary  circumference.  All 
these  tests  should  be  tried  at  first  with  each  eye  separately, 
while  the  other  is  closed,  and  then  with  both  eyes  open. 

The  Argyll-Robertson  pupil  responds  during  efforts  at 
accommodation,  but  not  to  light.  It  is  one  of  the  most 
important  signs  in  nervous  pathology,  as,  when  sight  is 
preserved,  it  is  only  found  in  locomotor  ataxia,  cerebral 
syphilis,  and  dementia  paralytica. 

Paralysis  of  the  ocular  muscles  may  be  at  once  apparent 
by  pronounced  deviation  of  one  or  both  eyes.  In  slighter 
degrees  its  presence  is  shown  by  the  patient's  inability  to 
perform  the  movements  controlled  by  certain  muscles.  It 
is  accompanied  by  double  vision. 

The  information  obtained  by  means  of  the  ophthalmo- 
scope is  always  valuable,  and  not  infrequently  permits  a 
diagnosis  which  otherwise  could  not  have  been  made.  In 
recommending  its  general  use,  however,  it  must  be  empha- 
sized that  it  is  an  instrument  requiring  considerable  skill 
and  constant  practice.  To  understand  the  significance  of 
the  pictures  which  it  reveals  implies  its  almost  daily  use  in 
both  health  and  disease.  In  the  hands  of  a  novice,  normal 
variations  may  be  regarded  as  evidences  of  morbid  con- 
ditions, and  pathological  changes,  significant  even  when 
slight,  may  escape  detection.  Few  general  practitioners 
have  the  opportunity  to  acquire  the  skill  which  is  neces- 
sary to  obtain  reliable  results  from  ophthalmoscopic  exami- 
nation, and  it  is  accordingly  advisable  to  have  their  ob- 
servations and  conclusions  submitted  to  the    control    of   a 


24 


INTRODUCTION. 


competent  ophthalmologist,  who  shall  at  the  same  time 
determine  refractive  errors  if  they  exist,  and  the  presence 
or  absence  of  such  insufficiencies  of  the  ocular  muscles  as 
only  appear  by  the  use  of  prisms. 

The  limits  of   the   field   of    vision  are    obtained   by  the 
perimeter.      The  use   of   this  instrument   requires    no  par- 
ticular skill.     It  is,   however,  a  too  frequently  for- 
gotten fact  that  perimetric  examinations  are  only 
of  value   when  supplemented  by  general  examina- 
tion of  the  eyes. 

A  limitation  of  the  visual  fields  can  only  be 
diagnosticated  as  functional 
when  examination  by  a  com- 
petent ophthalmologist  has 
proved ,  an  absence  of  or- 
ganic disease  or  defects 
which  might  explain  it. 

There  are  many  varie- 
ties of  perimeters,  of  which 
the  most  useful,  from  the 
neurologist's  standpoint,  is 
the  one  devised  by  Schweig- 
ger  (Fig.  i).  It  can  be  taken 
apart,  is  easily  portable,  and 
furnishes  sufficiently  accu- 
rate results.  This  instru- 
ment is  held  by  the  patient  so  that  the  cupped  end  of  the 
upright,  a,  is  placed  just  under  the  lower  rim  of  the  orbit, 
and  the  patient  is  directed  to  look  through  the  hole,  b. 
The  movable  arc,  c,  can  be  placed  at  will  at  different 
meridians,  which  are  indicated  by  the  pointer,  d.  The 
object  carrier,  e,  is  fitted  with  jaws,  into  which  can  be  in- 
serted the  disks  containing  little  squares  of  different  colors 
and  of  white.  In  examining  for  the  field  of  vision-  the  eye 
not  under  examination  is  covered,  and  the  object  is  removed 


Fig.  I. — Schweigger's  perimeter. 


THE    CRANIAL   NERVES. 


25 


from  the  periphery  of  the  field  toward  the  center.  As  soon 
as  it  is  perceived,  the  degree  is  read  from  the  scale  and  is 
marked  on  the  perimetric  chart. 

As  indicated  by  the  chart  (Fig.  2),  the  normal  field  of 
vision  for  white  on  the  horizontal  meridian  is  90°  on  the 
temporal  side,  and  60°  on  the  nasal  side  ;  on  the  vertical 
meridian  it  is  55°  superiorly  and  70°  inferiorly.  The  out- 
line of  the  entire  field  as  indicated  in  the  chart  is  fairly 
constant  in  normal  eyes.     It  is  subject  to  slight  variations 


L.JE;. 


B.K 


.^..^arr^ '    "^^TT^*^^^,,  ,,„„^.-rfir""' 


Fig.  2. — Normal  field  of  vision. 


in  different  individuals  within  normal  limits,  but  a  diminu- 
tion of  ten  degrees  must  be  regarded  as  of  pathological 
significance. 

The  fields  for  the  different  colors  are  smaller  than  those 
for  white.  They  range  in  size  from  the  field  for  blue,  the 
largest,  through  those  for  yellow,  orange,  red,  and  green  in 
the  order  named,  to  that  for  violet,  which  is  the  smallest. 
It  is  usually  convenient  to  limit  the  examination  of  the  color 
fields  to  those  for  blue  and  red. 

The  methods  of  examination  of  the  other  cranial  nerves. 


26  INTRODUCTION. 

with  the  exception  of  the  eighth  and  the  various  gustatory 
fibers,  will  be  found  in  the  description  of  their  injuries,  so 
that  they  need  not  be  given  here.  A  few  words  must  be 
said,  however,  regarding  the  senses  of  hearing  and  of  taste. 

Hearing. — Auditory  Nerve. — Tests  of  hearing  should 
be  made  for  one  ear  at  a  time,  the  other  ear  being  tightly 
closed.  Lesions  of  the  auditory  nerve  can  be  distinguished 
from  those  affecting  the  external  or  middle  ear  by  the  pres- 
ence or  absence  of  "  bone  conduction."  When  deafness  is 
the  result  of  inflammations  or  defects  which  affect  the  ear 
without  involving  the  auditory  nerve,  the  patient  can  hear 
the  tick  of  a  watch  or  the  sound  of  a  tuning  fork  when 
either  of  these  objects  is  placed  on  the  mastoid  process, 
very  much  better  than  when  it  is  held  directly  opposite 
the  auditory  meatus ;  on  the  other  hand,  when  the  audi- 
tory nerve  is  affected,  either  in  its  course  or  in  its  termi- 
nations  within  the  labyrinth,  the  deafness  is  equally  pro- 
nounced in  whichever  situation  the  testing  object  is  held. 
In  the  first  case,  in  which  the  auditory  passages  are  ob- 
structed, the  bone  conducts  the  sound  to  the  auditory 
nerve ;  in  the  second  case  it  is  the  nerve  itself  which  is 
affected,  and  deafness  consequently  exists  independently  of 
conduction. 

Taste. — The  sense  of  taste  depends  upon  several  nerves, 
and  it  is  rarely  if  ever  lost  as  a  result  of  organic  injuries 
which  do  not  cause  coma  or  extreme  laceration  of  the 
mouth  and  pharynx.  Flavors  are  recognized  by  means  of 
the  olfactory  nerve.  The  gustatory  function  has  to  do  with 
the  qualities  salt,  sweet,  bitter,  and  sour,  and  certain  me- 
tallic sensations  only. 

In  examination  for  the  sense  of  taste  the  test  solutions 
(sodium  chloride,  10  per  cent ;  sugar,  5  per  cent ;  tartaric 
acid,  10  per  cent;  strychnine,  o.i  per  cent)  are  applied  to 
the  tongue  by  means  of  a  glass  rod  while  the  patient's  eyes 
are  covered  and  his  nostrils  closed.     The  tongue  is  held 


PARALYSIS. 


27 


outside  the  mouth,  and  the  examiner  places  drops  of  the  test- 
ing fluids  on  it  and  inquires  if  the  patient  recognizes  them. 
The  examination  is  often  unsatisfactory.  Many  normal  per- 
sons can  not  taste  when  the  tongue  is  outside  of  the  mouth, 
yet  when  it  is  withdrawn  it  is  placed  against  the  palate,  and 
it  is  then  impossible  to  localize  gustatory  abnormities  if 
any  exist.  The  galvanic  current  is  a  preferable  means  of 
testing  for  disturbances  of  taste.  A  very  weak  current, 
such  as  may  be  obtained  from  a  single  cell,  is  made  to 
pass  through  the  tongue  from  wire  electrodes  placed  a 
short  distance  apart.  In  this  way  the  situation  of  any 
loss  of  the  ability  to  recognize  the  metallic  sensations  may 
be  discovered. 

Paralysis. — After  the  initial  shock  has  passed  away, 
paralysis  from  cerebral  lesions  is  rarely  absolute.  Even 
when  the  use  of  the  paralyzed  member  is  very  greatly  im- 
paired, the  patient  can  usually  succeed  in  producing  some 
flight  movement.  In  injuries  to  the  spinal  cord,  on  the 
other  hand,  complete  paralysis  is  the  rule,  so  that  the  limbs 
lie  useless  and  as  though  dead.  In  peripheral  nerve  lesions 
the  paralysis  is  so  distributed  that  some  muscles  may  be 
absolutely  paralyzed,  while  the  motor  power  in  others  is  as 
good  as  it  ever  was.  The  paralyses  of  hysteria  also  have 
characteristics  of  their  own. 

When  the  patient  is  unconscious,  the  examination  for 
paralysis  must  of  course  be  made  without  his  assistance.  If 
the  coma  is  not  profound,  he  may  be  seen  to  move  the  limbs 
of  one  side  while  those  of  the  other  side  remain  motionless  ; 
or  the  limbs  of  one  side  may  remain  unaffected  by  such 
peripheral  irritations  as  pricking,  pinching,  or  tickling — 
annoyances  which  the  limbs  of  the  other  side  endeavor  to 
escape.  Even  when  the  patient  is  absolutely  comatose,  by 
observing  differences  of  passive  muscular  resistance — such 
as  are  shown  by  the  way  in  which  the  limbs,  when  lifted  up, 
fall  again  to  the  bed,  or  by  the  condition  of  the  muscles  as 


28  INTRODUCTION. 

revealed  by  grasping  them  with  the  hand — the  physician 
can  usually  recognize  inequalities  of  muscular  power  on  the 
two  sides.  When  the  patient  is  able  and  willing  to  assist  the 
examiner,  the  task  is  much  easier.  If  the  loss  of  power  is 
complete  and  generall}^  distributed,  it  is  self-demonstrative  : 
but  if  partial,  or  if  limited  to  certain  muscles  or  groups  of 
muscles,  it  mav  require  considerable  care  and  skill  to  elicit 
its  exact  character.  The  object  may  best  be  accomplished 
by  directing  the  patient  to  perform  certain  movements  and 
to  repeat  them  in  rapid  succession,  and  to  make  all  the  re- 
sistance of  which  he  is  capable  against  the  force  exerted 
by  the  examiner.  In  this  way  may  be  found  not  only  the 
situation  of  the  paralysis  but  also  its  degree.  The  methods 
of  examination  for  paralyses  of  the  face  and  tongue  will  be 
described  when  speaking  of  those  affections. 

The  neck  is  rarely  the  seat  of  traumatic  paralysis.  Its 
presence  is  indicated  by  an  inability  to  move  the  head  and 
neck  in  the  various  directions,  or  b}'  abnormal  attitudes. 
To  detect  palsy  of  the  muscles  about  the  shoulder  joint,  the- 
patient  should  be  required  to  make  all  the  movements 
possible  at  this  point,  such  as  putting  the  hand  on  the  head,, 
the  chest,  the  opposite  shoulder,  and  the  back,  and  the  press- 
ing of  the  arm  firmly  against  the  side.  He  should  try  to 
maintain  these  positions  while  the  examiner  attempts  to 
overcome  them.  By  comparing  the  two  sides  in  this  way, 
degrees  of  relative  weakness  may  be  demonstrated.  Simi- 
lar procedures  are  applicable  at  the  elbow  and  wrist  joints. 
The  best  means  of  detecting  slight  degrees  of  paralysis  in 
the  extensors  and  fiexors  of  the  wrist  and  fingers  is  to  have 
the  patient  rapidly  open  and  close  the  hands  for  as  long  a 
time  as  he  is  able.  By  this  test  is  shown  unilateral  weak- 
ness as  well  as  the  stiffness  of  the  joints  which  is  so  impor- 
tant an  indication  of  certain  forms  of  injuries  to  nervous 
structures.  The  grip  may  be  tested  by  having  the  patient 
grasp  and  squeeze  with  both   hands  the  two  hands  of  the 


PARALYSIS. 


29 


examiner.  Weakness  in  the  interossei  and  lumbricales  is 
seen  by  impairment  of  the  finer  movements  of  the  fingers. 
The  patient  has  difficulty  in  buttoning  his  clothes,  in  pick- 
ing up  pins  or  other  fine  objects,  in  the  effort  necessary  to 
writing,  and  in  similar  movements  which  require  muscular 
strength  and  precision. 

The  examination  of  the  muscles  of  the  abdomen,  back^ 
and  lower  extremities  is  conducted  on  similar  lines.  The 
patient,  when  lying  at  full  length,  should  be  requested  to 
raise  himself  to  the  sitting  posture  without  using  legs  or 
arms ;  he  should  be  told  to  "  bear  down  "  while  the  hand 
of  the  examiner  is  on  the  abdominal  wall ;  he  should  be  ob- 
served while  getting  into  a  chair  and  while  getting  out  of 
it  without  using  the  hands.  The  movements  at  the  hip, 
knee,  and  ankle  joints  should  be  carefully  noted.  Assum- 
ing and  leaving  the  "squatting"  position  tests  the  muscles 
on  the  front  and  back  of  the  thigh  ;  they  may  also  be  tested 
by  stepping   with   one  leg   on  to  and   down    from    a   chair 


Fig.  3. — Hand  dynamometer. 

without  assistance.  The  muscles  of  the  legs  may  be  tried 
by  forward,  backward,  and  lateral  movements  of  the  foot. 
For  the  examination  of  these  motor  functions  various  instru- 
ments are  employed,  notable  among  which  is  the  hand  dy- 
namometer (Fig.  3),  used  to  determine  in  kilogrammes  or 
pounds  the  strength  of  the  grip.     Dana  has  devised  an  ap- 


20  INTRODUCTION. 

paratus  by  which  the  strength  of  the  muscles  of  the  lower 
extremities  may  be  similarly  measured.  While  these  instru- 
ments are  often  convenient,  they  are  by  no  means  essential 
for  securing  an  accurate  idea  of  the  muscular  power,  and, 
in  my  experience,  equally  reliable  results  may  be  obtained 
without  them. 

Rigidity. — The  rigidity  or  spasticity  which  appears  after 
lesions  of  the  central  neuron,  either  in  the  brain  or  in  the 
spinal  cord,  and  which  eventually  leads  to  contractures, 
begins  to  appear  in  a  few  weeks  after  the  receipt  of  the 
injury.  It  is  characterized  by  a  stiffness  of  all  the  muscles 
and  by  an  overaction  of  the  ones  which  are  the  least  para- 
lyzed. There  is  a  consequent  limitation  of  movement  at  the 
joints,  which  may  ultimately  render  them  absolutely  immo- 
bile. This  late  rigidit}^  is  unmistakable;  it  is  shown  by  the 
general  stiffness  of  movement,  and  especially  by  the  gait. 

Acute  cerebral  lesions  which  produce  paralysis  cause  ri- 
gidity in  the  paralyzed  limbs  at  once.  This  is  called  early 
rigidity,  and  is  indicative  of  an  irritative  lesion  of  the  upper 
motor  pathway.  When  the  loss  of  power  is  well  marked  it 
can  easily  be  detected  that  the  limbs  are  paralyzed  as  well 
as  stiff ;  but  it  not  infrequently  occurs  that  the  affected  limb 
is  rigid,  and  still  the  patient  can  move  it.  It  is  in  such 
cases  that  rigidity  is  an  important  diagnostic  symptom. 
Its  existence,  if  the  patient  is  conscious,  can  easily  be  dem- 
onstrated by  havmg  him  execute  rapid  movements  which 
require  a  considerable  flexibility  in  the  muscles,  and  ob- 
serving whether  they  are  done  with  normal  ease  and  speed. 
When  there  is  coma,  the  presence  of  the  rigidity  must  be 
determined  by  the  way  the  limbs  feel.  This  is  easy  to  do  if 
the  stiffness  is  pronounced,  as  the  limb  then  feels  abnor- 
mally hard  and  resistant  to  the  touch.  But  when  present  in 
slight  degree  only  it  is  usually  observed  by  no  one  except 
by  him  who  looks  for  it  carefully,  and  who  is  accustomed 
to  looking  for  it. 


DISORDEKS   OF    MOVEMENT,  3 1 

Tremor. — Tremor  of  the  face  is  observed  during  the  ex- 
amination of  the  head.  In  the  extremities  it  exists  chiefly 
in  the  arms  and  hands,  though  it  may  also  occur  in  the  legs. 
By  causing  the  patient  to  stand  with  his  arms  stretched  out 
in  front  of  him  and  his  fingers  spread  apart,  by  having  him 
execute  movements  with  the  arms  and  legs,  the  distri- 
bution and  character  of  the  tremor  may  be  ascertained. 
Tremor  of  the  hands  is  further  shown  by  the  handwriting; 
and  of  the  legs  in  attempts  made  by  the  patient  at  trying 
to  touch  objects  with  the  toes,  or  by  trying  to  describe  cir- 
cles on  the  floor. 

Fibrillary  tremor,  or  fibrillation,  is  a  very  fine,  rapid, 
wavelike  contraction  of  individual  muscle  fibers.  It  causes 
no  movement,  and  although  its  occurrence  is  involuntary 
it  is  often  observed  by  the  patient  himself.  It  is  seen 
chiefly  in  the  face,  in  the  muscles  around  the  shoulders,  and 
in  those  around  the  base  of  the  thumb.  Although  a  nearly 
constant  symptom  in  muscular  atrophy,  and  in  most  atro- 
phic spinal  cord  lesions,  it  is  not  pathognomonic  of  any 
disease,  as  it  may  occur  in  asthenic  conditions  which  are 
brought  on  by  excesses  of  any  kind. 

Morbid  Movements. — Convulsions,  athetosis,  spasmodic 
twitchings,  and  similar  purposeless  movements,  when  re- 
sulting from  accidents,  are  symptoms  of  so  pronounced 
a  character  that  there  is  rarely  any  difficulty  in  referring 
them  to  the  lesions  or  conditions  of  which  they  are  the 
results.  Unless  the  injury  has  been  extremely  severe,  the 
physician  only  occasionally  has  the  opportunity  of  wit- 
nessing these  symptoms.  In  making  his  decision  as  to 
their  character,  he  must  depend  largely  upon  information 
from  outside  sources.  In  hospitals,  where  the  patients  are 
under  the  constant  observation  of  the  house  staff  and  of 
trained  nurses,  there  can  be  no  question  as  to  the  reliabil- 
ity of  the  facts  reported  to  him.  But  in  the  absence  of 
observations  by  skilled   assistants  he  should   be  extremely 


22  INTRODUCTION. 

cautious  lest  he  attribute  too  much  weight  to  symptoms 
he  does  not  see. 

Gait. — If  the  patient  is  able  to  walk,  valuable  and  posi- 
tive information  concerning  the  condition  of  the  motor 
mechanism  may  be  obtained  by  the  observation  of  the  gait. 
Aside  from  such  individual  peculiarities  of  locomotion  as 
are  due  to  disorders  of  the  bones  or  joints,  there  are  certain 
types  of  gait  which  are  absolutely  typical  as  expressions  of 
morbid  conditions  which  can  never  be  successfully  simu- 
lated. 

The  Ataxic  Gait  is  the  most  characteristic  of  these. 
It  occurs  after  lesions  to  certain  sensory  fibers  and  is 
especially  seen  in  locomotor  ataxia.  In  that  disease  there 
is  no  loss  of  motor  power,  but  there  is  loss  of  the  sense  of 
position,  so  that  the  patient  does  not  walk  well  because  he 
does  not  know  where  to  put  his  feet.  More  force  than 
necessary  is  used  in  bringing  the  legs  forward  ;  the  feet  are 
lifted  too  high  and  thrown  too  far  outward,  and  finally  come 
down  to  the  floor,  the  heel  first  and  then  the  toe,  with  a 
sharp  slap.  In  slight  degrees  of  ataxia,  although  the  patient 
may  get  around  fairly  well,  and  can  often  walk  rapidly  and 
go  long  distances,  there  is  dif^culty  in  walking  in  the  dark, 
or  in  going  downstairs.  When  the  ataxia  is  more  pro- 
nounced, the  patient  walks  with  his  eyes  riveted  upon  his 
feet,  trying  in  this  way  to  direct  the  movements  of  the  legs. 
When  the  ataxia  is  still  more  exaggerated  the  patient  is 
only  able  to  walk  with  the  assistance  of  a  cane  or  of  an  at- 
'■  tendant,  or  locomotion  may  be  altogether  impossible. 

Gait  of  Motor  Paralysis. — The  gait  of  motor  paraly- 
sis has  essential  differences  according  to  whether  it  is  the 
central  or  peripheral  motor  neuron  which  is  affected. 

With  injury  to  the  central  motor  neuron,  the  paralysis 
is  usuall}'^  only  partial,  and  is  associated  with  stiffness ;  in 
lesions  of  the  peripheral  neuron  it  is  more  complete,  but 
the  muscles  are  soft  and  all  rigidity  in  them  is  absent. 


GAIT  oo 

The  types  of  gait  dependent  upon  affections  of  the  upper 
neuron  are  hemiplegia  and,  when  both  sides  are  affected, 
spastic.  The  hemiplegic  gait  is  usually  spastic,  but  the 
term  spastic  is  generally  understood  to  apply  to  cases  in 
which  both  legs  are  affected. 

Hemiplegic  Gait. — In  cerebral  hemiplegia,  after  the 
acute  effects  of  injury  have  passed  away,  the  leg  ordinarily 
regains  quickly  much  of  its  power,  but  the  descending  de- 
generation in  the  motor  pathway  causes  it  to  become 
very  stiff.  In  walking,  the  patient  throws  the  weight  of  the 
body  toward  the  unparalyzed  side  and  circumducts  the 
paralyzed  leg  so  that  it  describes  a  segment  of  a  circle  in 
its  forward  movement.  From  this  peculiarity  it  is  some- 
times called  the  "  mowing  gait."  The  foot  is  dragged  at  its 
tip  and  inner  portions  only,  and  there  is  little  movement  at 
the  knee  or  ankle  joints. 

Spastic  Gait. — The  spastic  gait  is  the  gait  of  double 
hemiplegia.  It  occurs  as  the  result  of  bilateral  lesions  of 
the  brain,  or  of  lesions  of  the  spinal  cord  above  the  lower 
dorsal  region. 

Its  characters  are  essentially  the  same  as  those  of  the 
hemiplegic  gait,  except  that  both  legs  are  involved  and  that 
the  degree  of  paralysis  is  greater  than  in  hemiplegia.  In 
walking,  the  patient  stiffly  circumducts  one  leg  until  the 
foot  has  crossed  in  front  of  the  foot  of  the  opposite  side. 
The  same  thing  is  then  done  with  the  other  foot.  From  this 
crossing  of  one  foot  in  front  of  the  other,  the  spastic  gait  is 
sometimes  called  "  crossed-leg  progression."  The  soles  of 
the  feet  leave  the  floor  but  little  or  not  at  all,  and  the  power 
of  locomotion  is  consequently  impaired  seriously.  If  the 
patient  carries  a  cane  he  keeps  it  in  front  of  him,  and  leans 
on  it  with  both  hands. 

The  Equine  Gait  is  the  type  of  gait  in  flaccid  paralysis 
of  the  anterior  tibial  group  of  muscles.  It  is  due  to  lesion 
of  the   peripheral  neuron,  and   is  seen   in  peripheral  nerve 


34 


INTRODUCTION. 


palsies  and  in  injuries  of  the  spinal  cord  in  or  below  the 
lumbar  enlargement.  It  is  never  associated  with  rigidity. 
As  a  result  of  the  paralysis,  when  the  lower  limb  is  raised 
the  foot  drops,  so  that  the  toe  touches  the  floor.  The  toe 
is  then  dragged,  or  the  leg  is  raised  higher  than  normal,  in 
order  that  the  foot  may  clear  the  floor.  There  is,  accord- 
ingly, pronounced  "  knee  action,"  and  hence  the  term  stepping 
or  equine  gait. 

In  addition  to  these  characteristic  and  constant  anoma- 
lies of  progression  there  are  other  disturbances  of  gait  which 
are  frequently  observed  and  which,  when  present,  are  at 
once  suggestive  of  the  conditions  to  which  they  are  due. 
Of  these  may  be  mentioned  the  careful  steps  of  the  patient 
with  lumbago ;  the  inert  dragging  of  the  feet  in  hysteria ; 
the  quick  yet  careless  walk  often  seen  in  the  early  stages  of 
dementia  paralj'tica  ;  and  the  festination  of  paralysis  agitans, 
of  which  Trousseau  said  that  "  the  patient  was  running  after 
his  center  of  gravity." 

Intimately  allied  to  the  gait  is  the  ability  of  the  patient 
to  maintain  his  equilibrium.  Normal  persons  can  not  hold 
themselves  perfectly  motionless  when  standing  with  closed 
eyes,  but  in  them  the  swaying  is  slight.  When  the  swaying 
is  pronounced  it  constitutes  a  symptom  of  importance  and 
is  called  the  Romberg  symptom. 

If  the  patient  is  in  bed  and  unable  to  use  his  legs  it  is,  of 
course,  impossible  to  make  these  tests.  But  many  persons 
remain  in  bed  for  long  periods  of  time,  although  they  are 
perfectly  able  to  walk.  It  is  always  desirable  to  have  the 
patient  make  the  attempt,  when  possible ;  when  this  is  not 
possible,  much  information  may  be  obtained  by  observing 
how  the  patient  lies  in  bed,  how  the  limbs  are  held,  and 
whether  their  attitude  indicates  pain. 

Sensation. — Although  the  clinical  value  of  the  anomalies 
of  cutaneous  sensation,  especially  as  observed  in  the  func- 
tional nervous  diseases,  has  been  subjected  to  much  adverse 


SENSATION.  35 

criticism,  the  fact  remains  that  anaesthesia,  whether  of  func- 
tional or  organic  origin,  is  one  of  the  most  valuable  aids  in 
neurological  diagnosis,  and  no  examination  of  a  nervous 
case  can  be  regarded  as  satisfactory  in  which  the  presence 
or  absence  of  ansesthesia  has  not  been  definitely  determined. 
For  sensory  examinations  there  are  a  variety  of  instruments 
vi^hich  are  of  greater  service  to  the  anthropologist  and  ex- 
perimental psychologist  than  to  the  clinician.  It  is  not  only 
usually  impossible  to  exercise  in  the  clinic  the  exactness  of 
the  laboratory,  but  it  is  generally  true  that  any  deviation 
from  normal  sensibility  is  of  very  questionable  clinical  value 
when  it  is  so  slight  as  to  require  instruments  of  precision  for 
its  determination. 

The  ccsthesiometer,  the  instruments  for  recording  de- 
grees of  pressure,  the  concealed  needles  for  testing  sensi- 
bility to  pain,  and  the  n^etal  piles  for  determining  the  de- 
gree of  thermo-ansesthes'ia  are  rarely  if  ever  necessary  in 
clinical  examinations  ;  a  needle,  a  piece  of  cotton,  and  two 
test  tubes,  one  filled  with  hot  and  the  other  with  cold  water, 
are  usually  sufficient  apparatus,  and  furnish  results  as  reli- 
able as  those  obtained  by  more  delicate  instruments. 

During  the  examination  the  patient's  eyes  are  covered, 
and  he  is  asked  to  indicate  when  he  feels  a  touch  rather  than 
if  he  feels  it.  It  is  advisable  from  time  to  time  for  the 
examiner  to  pretend  to  touch  the  patient  without  actually 
doing  so,  and  then  noting  whether  or  not  he  responds ;  for 
the  patient,  although  he  can  not  see,  may  say,  on  hearing 
the  rustle  of  the  coat  sleeve,  that  he  felt  contact  when  none 
was  made.  It  is  often  impossible  or  inadvisable  to  extend 
the  examination  over  the  whole  cutaneous  surface ;  the  re- 
port should  then  state  what  parts  were  not  examined  and 
the  reasons  for  the  omissions. 

The  limits  of  the  anaesthesia  are  usually  sharply  defined 
in  organic  cases.  In  functional  cases  the  boundary  between 
parts  which  are  ansesthetic  and  those  which  have  retained 


^5  INTRODUCTION. 

normal  sensibility  is  often  difficult  and  sometimes  impossible 
to  accurately  determine.  Inasmuch  as  a  thorough  examina- 
tion is  fatiguing  to  both  patient  and  examiner,  it  is  advisable 
in  such  cases  to  be  satisfied  with  an  approximation  of  the 
anaesthetic  limits  rather  than  to  overfatigue  the  patient,  be- 
cause if  he  becomes  tired  his  answers  are  less  reliable.  The 
results  of  sensory  examination  are  best  recorded  by  anges- 
thesia  charts,  which  are  printed  on  pads  with  gummed 
backs,  or  which  may  be  stamped  out  with  rubber  dies.  It 
is  most  convenient  to  mark  the  affected  areas  with  ink  or 
pencil  on  the  patient,  and  then  to  transfer  them  to  the 
chart.  Ansesthesia  of  different  characters  may  be  indicated 
by  vertical  or  horizontal  lines,  by  crosses  or  circles,  or  by 
various  other  devices. 

The  different  forms  of  sensibility  should  be  examined 
sequentially.  The  condition  of  the  sense  of  touch  of  the 
skin,  as  well  as  the  patient's  abihty  to  indicate  the  part 
touched,  is  ascertained  by  light  brushes  with  the  cotton. 
The  state  of  the  conjunctivse  and  the  lips,  tongue,  and 
throat  may  be  best  examined  at  the  same  time.  Slowed 
■conduction  is  essentially  a  symptom  of  chronic  processes. 

For  the  sense  of  pain,  examination  with  a  needle  fur- 
nishes the  desired  information  in  most  cases,  although  when 
simulation  is  suspected  other  devices  (see  Part  III)  are  some- 
times resorted  to.  In  testing  the  sense  of  temperature  two 
test  tubes,  one  filled  with  cold  water  and  the  other  with  water 
at  a  temperature  of  between  120°  and  130°,  will  enable  the 
physician  to  discover  any  differences  in  the  perception  of 
either  heat  or  cold,  as  well  as  the  patient's  inability  to  distin- 
guish between  these  two  varieties  of  sensory  stimulation. 

The  muscular  sense  is  a  complex  function,  and  is  usually 
abolished  when  ancESthesia  is  total.  It  includes  the  sense  of 
position  of  the  limb  and  the  appreciation  of  the  amount  of 
exertion  necessary  for  the  performance  of  voluntary  move- 
ments.    When  the  muscular  sense  is  lost  and  motor  power 


REFLEXES.  37 

is  retained,  the  patient,  in  attempting  movements  of  the 
limbs,  throws  them  about,  often  with  great  force,  but  with- 
out the  ability  to  properly  and  quickly  direct  them  toward 
the  objective  point.  This  condition  of  ataxia  is  seen  in  the 
gait  of  tabes,  and  may  be  demonstrated  for  the  upper  ex- 
tremities by  directing  the  patient  to  perform  definite  move- 
ments with  the  hands  and  observing  how  accurately  he  does 
them.  It  may  further  be  brought  out  by  attempts  of  the 
patient  to  put  the  limb  of  one  side  in  a  position  conforming 
to  that  in  which  the  limb  of  the  other  side  has  been  placed 
by  the  examiner,  or  by  his  inability  to  tell  with  closed  eyes 
the  exact  position  that  a  limb  is  in. 

Reflexes. — The  condition  of  the  pupillary  and  palpebral 
reflexes  are  determined  at  the  time  of  the  examination  of 
the  eye ;  the  pharyngeal  reflex  at  the  time  the  throat  is  ex- 
amined for  ansesthesia. 

There  remain  a  series  of  reflexes  termed  superficial,  and 
deep  or  tendon  reflexes,  which  should  be  examined  together. 
They  are  extremely  valuable,  and  often  constitute  the  one 
link  necessary  to  complete  the  diagnostic  chain.  The  most 
important  superficial  cutaneous  reflexes  are  the  cilio-spinal, 
those  of  the  abdomen,  the  cremasteric,  and  the  plantar. 

The  cilio-spinal  consists  in  a  dilatation  of  the  pupil  when 
the  skin  just  above  the  clavicle  is  irritated  by  pinching  or 
by  the  faradic  brush.  Its  loss  is  indicative  of  lesion  to  the 
cervical  sympathetic  or  to  the  first  dorsal  root,  or  to  the 
first  dorsal  segment  of  the  spinal  cord.  The  abdominal  re- 
flexes are  epigastric,  abdominal,  and  hypogastric.  Their 
action  in  health  is  seen  by  the  contractions  of  the  skin  in- 
duced by  quickly  stroking  these  regions  of  the  abdomen 
with  the  head  of  a  pin.  The  cremaster  reflex  occurs  as  the 
result  of  irritation  of  the  inner  side  of  the  thigh,  either  by 
striking  or  by  pinching,  which  causes  a  contraction  of  the 
cremaster  muscle  and  an  ascent  of  the  testicle.  In  the  plan- 
tar reflex,  irritation  of  the  sole  of  the  foot  causes  a  flexion 
4 


28  INTRODUCTION. 

at  the  knee  and  hip  joints  and  a  more  or  less  violent  agita- 
tion of  the  whole  limb. 

The  most  important  of  the  deep  or  tendon  reflexes  are 
those  concerned  in  the  contraction  of  the  triceps,  the  supina- 
tor longus,  the  biceps,  the  extensors  of  the  wrist,  and  the 
quadriceps  extensor  of  the  leg.  For  their  elicitation  it  is 
necessary  that  the  limb  be  pendent  and  free,  the  muscles 
relaxed,  and  that  light  taps  be  applied  over  the  tendons  of 
these  muscles,  preferably  with  a  small  hammer  provided 
with  a  rubber  tip,  known  as  the  plessimeter  (Fig.  4). 


Fig.  4. — Krauss's  plessimeter ;  by  unscrewing  the  caps  C  and  D  it 
may  be  used  as  an  £esthesiometer,  or  as  a  brush  for  testing  tactile 
sensibility. 

The  triceps,  or  elbow-jerk,  and  the  supinator  and  biceps 
reflex  are  not  necessarily  present  in  health,  although  they 
ma}^  be.  Their  presence  or  absence  is  readily  determined 
by  taps,  applied  for  the  former  just  above  the  olecranon  pro- 
cess, and  for  the  latter  (Fig.  5)  just  above  the  head  of  the 
radius  on  its  outer  surface. 

The  knee-jerk,  or  patellar  or  quadriceps  reflex,  is  by  far 
the  most  important  of  all.  In  health,  a  light  tap  upon  the 
patellar  tendon  induces  a  quick  but  slight  extension  of  the 
leg.  The  action  is  said  to  be  hypertypical  when  it  can  be 
elicited  by  taps  on  the  muscle  above  the  knee.  There  is  no 
absolute  standard  by  which  it  may  be  determined  when  a 
hypertypical  knee-jerk  becomes  exaggerated.  Very  great 
exaggeration  is  frequently  associated  with  ankle  clonus,  and 
even  in  the  absence  of  clonus,  when  light  taps  bring  about 
quick  and  forcible  muscular  contraction,  the  condition  must 
be  regarded  as  exaggerated.     Since  absence  of  knee-jerk  is 


REFLEXES. 


39 


occasionally  observed  in  persons  who  are  apparently  normal, 
this  symptom  alone  is  not  sufficient  for  the  diagnosis  of 
disease. 

When  the  examination  has  not  been  painstaking  it  may 
be  concluded  that  the  knee-jerk  is  absent,  although  the  em- 
ployment  of   the    proper   means   for   its   elicitation    would 


Fig.  s. — Showing-  method  of  obtaining  the  triceps  and  supinator  jerk. 


have  demonstrated  its  presence.  Such  an  error  is  particu- 
larly frequent  when  the  reflex  activity  is  diminished,  either 
as  a  personal  peculiarity  or  as  a  result  of  disease. 

In  the  larger  number  of  cases  this  reflex  may  be  obtained 
by  having  the  patient  sit  in  a  chair,  one  leg  crossed  over  the 


40 


INTRODUCTION. 


Other,  while  the  physician  taps  the  patellar  tendon.  If 
there  is  no  response,  the  Jendrassik  (Fig.  6)  method  of  re- 
enforcement  is  resorted  to.  The  patient,  having-  crossed 
the  legs,   pulls  forcibly  on  his  closed  hands  and  looks  up 


Fig.  6. — Showing  the  Jendrassik  method  of  obtaining  the  knee-jsrk. 


at  the  ceiling.  Before  striking  the  tendon  the  examiner 
should  satisfy  himself  that  the  patient's  hamstring  muscles 
are  relaxed. 

If  none  of  these  methods  is  successful  they  may  be  va- 
ried by  having  the  patient  sit  on  a  table  so  that  the  legs 
hang  over  the  edge  ;  or  the  examiner  may  place  one  arm 
under  the  leg  to  be  examined,  so  that  the  hand  rests  on 
the  knee  of  the  opposite  leg.     In  this  way  the  leg  is  ele- 


TROPHIC    DISTURBANCES. 


41 


vated  from  the  floor,  and  at  the  same  time  the  condition  of 
the  hamstring  muscles  is  ascertained. 

If  the  leg  is  held  perfectly  limp  and  no  reflex  can  be 
obtained  by  any  of  these  methods,  it  is  fair  to  infer  that  the 
knee-jerk  is  lost.  Such  an  inference  is  not  justifiable,  how- 
ever, if  the  flexor  muscles  of  the  legs  can  not  be  made  to 
relax,  as  sometimes  occurs  in  persons  who  persistently  re- 
fuse to  understand  what  is  said  to  them.  For  such  cases 
the  most  that  can  be  said  is  that  the  knee-jerk  was  not  ob- 
tained. 

Foot  or  Ankle  Clonus  is  usually  regarded  as  an  evidence 
of  degeneration  of  the  pyramidal  tracts,  although  it  may 
rarely  occur  in  functional  cases.  In  these  latter,  however,  it 
does  not  present  the  exaggerated  characteristics  which  stamp 
it  as  a  symptom  of  organic  disease.  To  examine  for  it  the 
patient  sits  down  and  the  examiner  supports  the  under  sur- 
face of  the  knee  with  the  left  hand  and  grasps  the  toes  with 
the  right.  The  foot  is  then  sharply  flexed.  If  ankle  clonus 
is  present,  there  ensues  a  series  of  rapidly  alternating  con- 
tractions of  the  flexors  and  extensors  of  the  ankle. 

Trophic  Disturbances. — Trophic  disturbances  of  the  skin 
become  at  once  apparent  when  the  cutaneous  surface  is  ex- 
posed ;  but  by  inspection  alone  it  is  impossible  to  determine 
the  presence  of  atrophy  of  the  muscles,  unless  it  has  already 
reached  a  considerable  degree  of  advancement.  Under 
such  circumstances  the  affected  part,  as  determined  by  in- 
spection or  by  measurement  with  a  steel  tape,  is  found  to  be 
smaller  than  that  of  its  fellow  of  the  opposite  side ;  or,  if 
both  limbs  are  involved,  smaller  than  there  is  reason  to 
suppose  they  were  before  the  accident.  Also,  when  the 
atrophy  of  muscle  is  pronounced,  the  skin  over  it  is  loose 
and  flabby,  and  there  is  absent  the  feeling  of  firmness  and 
resistance  characteristic  of  normal  muscle ;  but  in  the  early 
stages  such  unmistakable  evidences  of  atrophy  are  often 
wanting,  and   it  is   necessary   to   resort  to   examination   by 


42 


INTRODUCTION. 


electricity.  If  there  are  abnormal  changes  in  electrical  ex- 
citability it  follows  as  an  inevitable  conclusion  that  there  is 
also  an  atrophy  of  muscle,  although  it  may  have  escaped 
detection  by  other  methods  of  examination. 

Electrical  Examination. — In  cerebral  injuries  it  is  often 
immediately  evident  that  the  battery  can  throw  no  light 
upon  the  character  or  situation  of  the  lesion.  Electrical 
examination  is  indispensable  for  all  affections  of  the  lower 
motor  neuron,  and  no  case  of  paralysis  can  wath  justice  be 
diagnosticated  as  functional  unless  such  means  of  investiga- 
tion have  been  employed. 

Much  information  can  be  obtained  from  a  simple  faradic 
battery,  although  it  is  usually  desirable  to  test  with  both 
the  interrupted  and  the  constant  current.  The  sponges  in 
the  electrodes  must  be  kept  constantly  moist,  and  one  of 
them  should  have  a  small  head  and  be  furnished  with  an 
interrupter.  A  galvanometer  is  a  useful  addition  to  the 
galvanic  battery,  but  it  is  indispensable  only  when  the  pa- 
ralysis is  bilateral,  so  that  the  reactions  on  the  injured  side 
can  not  be  compared  with  those  of  the  opposite  (normal) 
side,  and  when  the  increased  strength  of  current  needed  to 
cause  contraction  is  the  only  index  of  trophic  change. 

The  reactions  of  degeneration  which  occur  after  lesions 
of  the  peripheral  neuron  are  essentially  the  same,  whether 
the  injury  has  occurred  in  the  spinal  cord  or  after  the 
nerves  have  made  their  exit.  Degenerative  reactions  are 
the  expressions  of  the  abolition  of  trophic  function  whose 
center  is  in  the  anterior  horns,  and  whether  it  is  the  center 
itself  which  is  destroyed,  or  the  means  of  transmission  of 
its  influence,  makes  no  difference  as  far  as  the  electrical  re- 
actions are  concerned. 

To  determine  the  character  of  these  changes  it  is  neces- 
sary to  examine  the  nerve  trunk  and  its  branches  to  the 
individual  muscles.  With  an  electrode  on  the  sternum  or 
some    other   indifferent    point,   the    examining   electrode    is 


-Abd.  dig.  min 
Fig.  7. — Diagram  showing  the  superficial  posilion  of  the  large  nerve  trunks  and  the  motor  points  for  the  muscles. 


ELECTRICAL    EXAMINATION. 


43 


placed  over  the  nerve  trunk  at  some  point  in  its  course. 
The  points  of  entrance  of  the  branches  to  the  muscles  were 
first  fully  ascertained  by  Erb,  and  their  topographical  dis- 
tribution is  shown  in  the  accompanying  chart  (Fig.  7). 

The  variations  in  the  character  of  electrical  responses 
■depend  upon  the  part  examined  (nerve  or  muscle),  the 
current  used,  the  extent  of  injury,  and  the  time  which  has 
elapsed  since  its  receipt. 

In  the  trunk  of  an  injured  nerve  changed  electrical  re- 
actions are  of  essentially  the  same  character  to  both  con- 
stant and  induced  current.  There  may  be  for  a  day  or  two 
after  the  injury  an  increase  of  excitability,  but  this  is  soon 
replaced  by  a  diminished  response,  and  in  the  course  of  a 
few  weeks  there  may  be  no  response  at  all.  If  recovery 
occurs  (and  the  loss  of  electrical  excitability  in  the  nerve 
trunk  does  not  imply  that  the  degeneration  is  irreparable), 
the  reaction  to  stimulation  will  be  gradually  restored. 

The  abnormal  electrical  reactions  of  the  nerve  termina- 
tions in  the  muscles  are  found  by  placing  one  electrode 
over  an  indifferent  point  and  the  examining  electrode  over 
the  motor  points  of  Erb,  which  correspond  in  position  with 
the  entrance  of  the  nerve  ending  into  the  muscle. 

At  these  points  the  electrical  evidence  of  nerve  injury 
differs  with  the  two  currents.  Response  to  the  faradic 
current  may  be  hyperactive  for  a  day  or  two  after  the 
injury,  but  it  then  rapidly  decreases  until  about  the  sec- 
ond week ;  then  there  is  no  longer  any  response  at  all. 
When  regeneration  begins,  often  about  the  second  month 
after  injury,  there  occurs  a  gradual  return  of  faradic  excita- 
bility. 

The  galvanic  reaction,  on  the  other  hand,  after  a  da)^  or 
two  of  normal  or  increased  response,  falls  with  the  faradic ; 
but  instead  of  becoming  extinct,  like  the  faradic,  it  begins  to 
rise  in  the  second  or  third  week.  The  increased  response  to 
galvanism   may   become  and   remain  so   marked  that  very 


44 


INTRODUCTION. 


weak  currents  produce  forcible  contractions.  The  increase 
of  galvanic  exxitability  may  persist  for  many  months  and 
eventually  be  replaced  by  total  absence  of  response  ;  or 
about  the  same  time  that  the  muscles  show  a  return  of  con- 
tractibility  to  faradism  the  galvanic  response  decreases  until 
it  reaches  and  remains  at  the  standard  of  health. 

The  accompanying  diagram  \Fig.  8)  may  graphically 
represent  the  behavior  of  the  electrical  reactions  for  the 
first  four  weeks  after  a  moderately  severe  injury  of  a  periph- 


IN   MUSCLE 

WEEKS  12  3  4 


IN   NERVE 
1  2  3 


NORMAL 

FARADIC 


WEEKS  I 


GALVANIC 


2         3  4 


Fig.  8. — Diagjam  to  illustrate  the  electrical  reactions  occurring  in  a  nerve  after  a 

moderately  severe  injury. 

eral  nerve.  It  is  seen  that  in  the  muscle  the  response  to 
faradism  is  hyperactive  for  a  few  days,  then  rapidly  sinks  in 
about  the  second  week.  The  galvanic  curve,  on  the  other 
hand,  after  an  initial  rise  and  fall,  begins  to  rise  after  the 
second  week,  and  remains  for  some  time  above  the  normal. 
In  the  nerve  the  behavior  of  the  two  currents  is  seen  to  be 
the  same. 

These  changes  in  electrical  reactions  indicate  degenera- 
tive processes  of  greater  or  less  severity  in  the  nerve  trunk 
and  nerve  endings.  They  are  quantitative.  Still  more  im- 
portant are  the  qualitative  changes  as  seen  in  the  "  reaction 
of  degeneration." 

The  reaction  of  degeneration  is  found  in  the  muscles 
only,  and  consists  in  a  reversal  of  the  normal  reaction  to 
galvanism. 


ELECTRICAL    EXAMINATION. 


45 


In  health  the  contraction  induced  by  closing  the  circuit 
is  greater  when  the  cathode  is  over  the  motor  point  than 
when  the  circuit  is  completed  with  the  anode  in  that  situa- 
tion. The  cathode-closure  contraction  is  greater  than  anode- 
closure  contraction,  or,  graphically  : 

CaCl  >  AnCl. 
In  disease  these  reactions  may  be  reversed,  so  that 

CaCl  =  AnCl, 
or  CaCl  <  AnCl. 

In  degeneration  of  nerves  the  contractions  of  the  mps-., 
cles  to  both  galvanic  and  faradic  currents  are  often  slow  and 
wormlike,  instead  of  being  quick  and  tonic,  as  in  health. 
This  vermicular  reaction,  like  the  reaction  of  degeneration, 
is  indicative  of  serious  though  not  necessarily  irreparable 
injury.  Such  are  the  changes  in  electrical  response  most 
frequently  observed  after  nerve  injuries. 


PART    I. 

ORGANIC  EFFECTS   OF  INJURY   TO    THE 
NERVOUS  SYSTEM. 

While  it  is  not  the  chief  object  of  this  work  to  portray 
the  clinical  or  pathological  conditions  which  may  result 
from  organic  injuries  to  the  nervous  system,  a  brief  men- 
tion of  nervous  symptoms  as  caused  by  definite  lesions  seems 
imperative  as  a  preliminary  to  the  study  of  functional  de- 
rangements. In  all  cases  of  traumatic  nervous  disease  the 
question  at  once  arises  whether  there  is  a  lesion  destroying 
nerve  tissue,  or  whether  the  symptoms  are  merely  indicative 
of  a  repression  or  perversion  of  function  of  temporary  char- 
acter occurring  independently  of  known  lesion. 

In  functional  cases  the  evidences  of  structural  lesion  are 
not  present ;  to  prove  them  absent,  however,  requires  a 
painstaking  examination  directed  toward  the  whole  cerebro- 
spinal axis.  It  is  accordingly  the  object  of  the  three  im- 
mediately succeeding  chapters  to  briefly  describe  the  symp- 
toms which  are  to  be  regarded  as  indicative  of  acute  or- 
ganic injury  to  the  brain,  the  spinal  cord,  and  the  peripheral 
nerves.  In  the  fourth  chapter  of  this  section  are  considered 
the  possibilities  for  a  traumatic  origin  of  certain  of  the 
chronic  degenerative  diseases. 

CHAPTER   I. 

INJURIES   TO   THE   BRAIN. 

Contrasted  to  the  cerebral  injuries  in  which  there  is  no 
difficulty  in  deciding  upon  the  character  or  the  approximate 
location  of  the  trouble,  are  cases  in  which  the  nature  or  even 


INJURIES   TO   THE    BRAIN.  47 

the  situation  of  the  lesion  can  not  be  determined  without  an 
examination  of  the  whole  nervous  system,  and  it  is  in  such 
cases  especially  that  the  physician  needs  to  be  familiar  with 
the  essential  characteristics  of  those  symptoms  which  be- 
speak loss  of  continuity  in  cerebral  conducting  paths  or  in- 
jury to  cerebral  cells. 

Even  the  most  scrupulous  care  and  widest  experience 
are  often  unavailing  for  diagnosis,  and  the  nature  of  the  con- 
dition does  not  become  plain  until  recovery  stamps  it  with 
characteristics  of  individual  types,  or  until  the  pathologist 
gives  the  answer  to  the  riddle  which  the  clinician  was  un- 
able to  solve. 

The  most  perplexing  cases  are  those  in  which  unknown 
persons  are  found  lying  senseless.  The  presence  of  scalp 
wounds  may  prove  a  head  injury,  such  as  could  have  been 
inflicted  by  a  blow  or  a  fall ;  witnesses  are  wanting,  and  the 
physician  or  surgeon  must  rely  upon  his  own  skill  to  decide 
whether  the  patient  lost  consciousness  as  the  result  of  a  fall 
or  blow  on  the  head,  or  whether  the  fall  resulted  from  dizzi- 
ness or  unconsciousness  brought  about  by  some  purely  medi 
cal  disease. 

It  is  the  old  and  perplexing  question  of  the  differential 
diagnosis  of  coma ;  its  consideration  here  must  be  limited 
to  a  brief  description  of  those  symptoms  which  are  usually 
present  when  it  is  due  to  direct  injury  of  cerebral  tissue. 
They  are  of  three  classes : 

1.  General,  which  may  occur  after  any  severe  general  in- 
jury. 

2.  Mental,  which  indicate  interference  with  intellectual 
processes. 

3.  Focal,  which  are  due  to  lesions  of  circumscribed  areas 
of  the  brain. 

I.  General  Symptoms. — The  most  important  symptom  of 
general  injury,  either  to  the  nervous  system  or  to  other 
parts,  is  surgical  shock. 


48  ORGANIC   EFFECTS   OF   INJURY. 

It  is  to  be  distinguished  from  psychic  or  nervous  shock, 
which  is  the  impression  made  upon  the  mind  by  sudden  and 
painful  emotional  influences.  Physical  or  corporeal  shock 
is  a  sudden  depression  of  the  functional  activity  of  the  gen- 
eral nervous  system.  Its  pathology  is  unknown.  It  is  a 
constant  accompaniment  of  severe  injuries  of  any  part,  and 
it  sometimes  follows  traumatism  of  a  trifling  nature.  It 
occurs  immediately  after  the  accident,  and  may  continue  a 
varying  length  of  time.  Consciousness  is  not  lost,  but  the 
patient  is  depressed  and  apathetic.  The  face  is  pale,  the  skin 
is  moist  and  cold,  the  pulse  is  soft,  rapid  and  feeble,  and  the 
respirations  are  shallow.  Shock  often  appears  to  be  the  sole 
determining  cause  of  death. 

Among  other  common  general  symptoms  of  lesion  to  the 
brain  more  suggestive  than  shock  may  be  mentioned  vomit- 
ing, slow  pulse,  stertorous  breathing,  the  tendency  to  con- 
gestion, oedema  or  consolidation  of  the  lungs,  fever,  and 
incontinence  or  retention  of  urine  or  faeces. 

2.  Mental  Symptoms. — Mental  symptoms  are  naturally 
the  most  prominent  evidences  of  disturbances  of  the  organ 
which  is  the  seat  of  the  intellectual  faculties.  In  injuries  to 
the  spinal  cord,  or  to  the  peripheral  nerves,  consciousness  is 
usually  retained  ;  but  in  all  severe  cerebral  injuries,  and  in 
many  which  are  apparently  trivial,  it  is  more  or  less  com- 
pletely lost.  The  term  "  coma  "  is  applied  to  the  condition 
in  which  the  patient  is  completely  unconscious,  and  can  be 
aroused  but  little  or  not  at  all  by  peripheral  irritations.  In 
the  milder  degrees  of  insensibility,  when  he  can  be  made  to 
answer  questions,  it  is  called  "stupor."  From  the  presence 
of  unconsciousness  alone,  it  is  usually  impossible  to  deter- 
mine whether  or  not  there  has  been  a  gross  structural  lesion 
of  the  brain.  After  a  blow  on  the  head  a  man  may  remain 
unconscious  for  several  days,  and  finally  recover  without 
any  further  evidences  of  cerebral  trouble ;  or  the  coma  fol- 
lowing a  similar  accident  may  be  less  profound,  although 


INJURIES   TO   THE   BRAIN.  49 

permanent  paralysis,  mental  impairment,  or  death  is  to  be 
the  result. 

Often,  instead  of  unconsciousness  or  hebetude,  the  mental 
condition  is  one  of  confusion.  This  may  even  be  the  case 
after  injuries  which  are  soon  to  prove  fatal. 

A  short  time  ago  I  had  the  opportunity  of  examining  at  the 
Harlem  Hospital  a  young  man  who  had  been  struck  by  a  billiard 
cue  over  the  right  parietal  eminence.  There  was  a  scalp  wound 
over  the  place  where  he  had  been  hit,  but  no  discoverable  evi- 
dences of  fracture.  At  the  time  I  saw  the  patient,  two  days  before 
his  death  and  several  days  after  the  accident,  he  was  apparently 
entirely  conscious  although  very  much  confused.  He  under- 
stood everything  that  was  said  to  him,  but  it  was  difficult  to  hold 
his  attention ;  when  told  to  put  out  his  tongue  or  perform  other 
acts,  he  obeyed  promptly,  but  he  did  not  seem  to  know  what  he 
was  doing,  and  had  to  be  spoken  to  two  or  three  times  before  he 
executed  the  movement.  There  was  general  increase  of  the  deep 
reflexes,  but  there  was  a  total  absence  of  evidences  of  local  injury 
to  the  brain.  Soon  after  this  he  became  comatose  and  died. 
The  autopsy  showed  a  fissured  fracture  of  the  right  parietal  bone, 
and  a  large  subdural  hsemorrhage  on  the  opposite  side  of  the 
brain. 

Delirium  is  a  frequent  complication  of  head  injuries, 
especially  in  alcoholic  persons.  It  may  be  mild  or  mutter- 
ing, or  may  be  attended  with  hallucinations,  delusions,  and 
impulsive  acts. 

None  of  the  mental  symptoms  of  head  injuries  is  neces- 
sarily indicative  of  permanent  organic  brain  lesion,  although 
it  is  generally  true  that  the  more  serious  the  mental  symp- 
toms the  more  probable  becomes  the  existence  of  some 
irremediable  cerebral  condition.  In  some  fatal  cases  of  trau- 
matic cerebral  haemorrhage  mental  symptoms  exist  without 
any  focal  signs. 

3.  Focal  Symptoms. — The  most  certain  and  definite  in- 
formation concerning  injuries  to  the  brain  is  furnished  by 
the  symptoms  of  lesions  confined  to  circumscribed  areas 
(see  Figs.  9  and  10).     Although  no  individual  region  of  the 


50 


ORGANIC   EFFECTS   OF   INJURY. 


brain  acts  independently  of  other  parts,  there  are  certain 
districts  which  have  specialized  functions,  and  injury  to 
these   causes   definite   and   constant  symptoms.      The   most 


Superior  frontal  sulcus. 


Fissure  of  Rolando. 


Interparietal  sulcus 


Ascending  ramus 
of  the  fissure 
of  Sylviub. 

Fissure  of 
Sylvius. 


Posterior  ramus  of  the 
fissure  of  Sylvius. 


Superior  temporal 
sulcus. 


Fig.  9. — Schematic  representation  of  the  cerebral  cortex  and  its  centers. 
(After  Tillmanns. ) 


1.  First.  ) 

2.  Second.      >  Frontal  convolution. 

3.  Third.        ) 


4.  Anterior. 

5.  Posterior. 

6.  Upper. 

7.  Middle. 

8.  Lower. 

g.  Upper. 
10.  Lower. 


Central  convolution. 


-Temporal  convolution. 


Parietal  convolution. 


11.  (jyrus  angularis. 

12.  Upper.       ) 

13.  Middle.      >  Occipital  convolution. 

14.  Lower.       ) 


O  In  4  and  5  on  both  sides  of  the  fissure  of 
Rolando,  motor  area  for  the  upper 
extremity. 

Q  Motor  area  partly  for  the  upper  and  part- 
ly for  the  lower  extremity  (great  toe). 

%  Motor  area  for  the  lower  extremity. 

©  Cortical  area  for  the  hypog;lossal  nerve. 

©  Cortical  area  for  the  facial  ner\'e. 

O  (3)  Motor  aphasia. 

X  (6)  Sensory  (auditor)')  aphasia  with 
word-deafness. 

■f»  (11)  Aphasia  with  word-blindness. 

•  (i2'l  Region  of  the  visual  area  (see  also 
Fig.  10). 


sharply  limited  of  these  districts  are  the  ones  which  preside 
over  the  faculty  of  speech  and  the  ones  concerned  in  vol- 
untary motion. 


INJURIES   TO   THE    BRAIN. 


51 


Speech  Disturbances. — Most  traumatisms  which  act  on 
the  brain  in  a  way  to  abolish  or  impair  the  activity  of  the 
centers  of  speech  cause  at  the  same  time  such  pronounced 

S.c. 


\  F.po. 


F.l. 


Fig.  10. — View  of  the  right  cerebral  hemisphere  from  the  median  side  ;  B,  corpus  callo- 
sum  divided  longitudinally;  G.f,  gyrus  fornicatus  ;  //,  gyrus  hippocampi;  S.  h.^ 
sulcus  hippocampi ;  G.  it. ,  gyrus  uncinatus  ;  6".  c.  m.,  sulcus  calloso-marginalis  ;  F.  /, 
first  frontal  convolution  ;  Ji".  c. ,  termination  of  the  fissure  of  Rolando  ;  in  front  the 
anterior  central  convolution  with  the  motor  area  partly  for  the  upper  and  partly  for 
the  lower  extremity,  and  behind  the  posterior  central  convolution  with  the  motor 
area  for  the  lower  extremity ;  P,  prajcuneus ;  C,  cuneus ;  F.po  ,  parieto-occipital 
sulcus  ;  /,  polus  ;  F.c,  calcarine  fissure  ;  in  the  posterior  part  of  this  the  visual  area 
is  shown  by  a  red  dotted  line.     (After  Tillmanns.) 

mental  symptoms  that  examination  for  the  highly  specialized 
cerebral  functions  is  unsatisfactory  or  unavailing-.  How- 
ever, as  such  selective  injuries  sometimes  occur  without  seri- 
ously interfering  with  general  intellectual  power,  and  since, 
when  the  acute  general  effects  of  injury  have  passed  away, 
there  may  be  left  symptoms  of  focal  lesions  to  parts  con- 
cerned in  the  faculty  of  language,  the  most  common  forms 
of  cerebral  speech  disturbances  must  be  mentioned. 

The  best  defined  of  the  cerebral  centers  for  speech  may 
be  seen   in  the  accompanying  figures  9  and   10.     They  in- 


^2  ORGANIC  EFFECTS  OF  INJURY. 

elude  the  second  and  third  left  frontal  convolutions,  injury 
to  which  causes  motor  aphasia  or  an  abolition  of  the  power 
of  voluntary  speech  without  paralysis  of  the  muscles  of 
articulation,  or  without  loss  of  understanding  of  spoken  or 
written  language.  Motor  aphasia  is  the  most  common  of 
the  isolated  speech  disturbances  which  may  be  due  to  trau- 
matisms. It  is  almost  always  associated  with  right  hemi- 
plegia. Injury  to  the  first  or  second  left  temporal  convolu- 
tion causes  word  deafness  or  the  loss  of  understanding  of 
spoken  words,  without  any  disturbance  of  hearing  or  with- 
out serious  impairment  of  the  power  of  speech.  Injuries 
to  the  occipital  lobes  sometimes  cause  a  loss  of  power  of  the 
understanding  of  written  signs,  and  if  situated  unilaterally 
near  the  calcarine  fissure,  hemianopsia.  Mind  blindness  and 
mind  deafness  are  rare  conditions,  in  which,  without  other 
mental  defect,  there  is  an  inability  to  recognize  familiar  ob- 
jects or  sounds. 

Motor  Symptoms. — Paralysis.— Loss  of  power  of  volun- 
tary movement  is  the  most  constant  and  mo§t  valuable  sign 
of  focal  injury  to  the  brain.  It  is  a  very  frequent  accom- 
paniment of  cerebral  traumata,  and,  even  when  slight  in  de- 
gree, its  meaning  is  so  unmistakable  that  examination  for  it 
should  be  scrupulously  made  in  all  cases,  although  it  may 
seem  at  first  to  be  absent.  The  nature  of  paralysis  may  be 
best  understood  by  referring  to  the  way  in  which  voluntary 
movements  are  normally  performed. 

Voluntary  movements  are  presided  over  by  the  motor 
cells,  which  are  situated  in  the  gray  matter  around  the 
fissure  of  Rolando.  It  is  in  the  cells  of  this  region  that  the 
motor  pathway  has  its  beginning,  and  the  motor  pathway 
(Fig.  ii)  is  the  cerebro-spinal  tract  of  which  our  knowledge 
is  most  complete. 

It  descends  through  the  brain  as  a  well-defined  bundle 
of  nerve  fibers  which  terminate  in  the  basal  ganglia,  the 
pons,  the  medulla,  and  the  anterior  horns  of  the  spinal  cord. 


INJURIES   TO   THE    BRAIN, 


53 


Before  reaching  the  spinal  cord  the  larger  number  of  these 
libers  decussate ;  those  for  the  cranial  nerves,  in  the  pons 
and  in  the  upper  part  of  the   medulla,  and   those   for  the 


lower  extremity 


Fig.  II. — Schema  illustrating  the  course  of  the  cerebro-spinal  motor  path. 
(After  Van  Gehuchten.) 

spinal  cord,  in  the  lower  part  of  the  medulla.  By  this  cross- 
ing, the  cerebral  fibers  for  motion  have  their  termination  in 
the  opposite  side  of  the  cerebro-spinal  axis  to   that  from 


54 


ORGANIC  EFFECTS  OF  INJURY. 


CORTEX 


CENTRAL 
NEURON 


which  they  came.  The  continuation  of  the  motor  tract  from- 
the  gray  matter  of  the  brain  axis  and  spinal  cord  is  in  the 
peripheral  nerves,  which  are  distributed  to  the  muscles. 

The   entire    tract  for  voluntary   motion,  from   cortex  to 
periphery,   is  composed  of  aggregations  of  nervous  units, 

which  are  called 
motor  neurons.  A 
neuron,  a  term  pro- 
posed by  Waldey- 
er  to  include  the 
nerve  cell  in  its  en- 
tirety, consists  of 
the  {a)  cell  body,, 
the  {b)  protoplas- 
mic processes  or 
dendrites,  which 
are  generally  sup- 
posed to  convey 
impulses  to  the 
cell  and  are  conse- 
quently afferent, 
and  the  (c)  axis 
cylinder  of  the 
cell,  or  the  neurax- 
on,  which  is  known 
to  convey  impulses 
from  the  cell  and 
is  consequently  efferent.  The  cerebro-spinal  motor  path- 
way is  principally  made  up  of  two  sets  of  these  neural  ele- 
ments, which  are  called  respectively  central,  upper,  or  sec- 
ondary neurons,  and  peripheral,  lozver,  or  primary  neurons 
(Fig.  12).  The  cell  body  of  the  central  neuron  is  situated  in 
the  motor  cortex  of  the  brain,  and  its  neuraxon  descends 
through  the  motor  pathway,  to  be  connected  by  fine  ter- 
minal filaments  with  the  peripheral  neuron.     The  peripheral 


MUSCLE 


Fig.  12.— Schema  to  illustrate  the  arrangement  of  the 
motor  neurons. 


INJURIES   TO    THE    BRAIN.  55 

neuron  connects  the  gray  matter  of  the  brain  axis  or  of  the 
spinal  cord,  as  the  case  may  be,  and  the  periphery.  Its 
body  is  in  the  gray  matter,  where  it  is  closely  associated 
with  the  terminations  of  the  central  neuron ;  its  heuraxons 
form  the  motor  fibers  of  the  peripheral  nerves.  A  volun- 
tary movement  is  the  result  of  some  change,  the  nature  of 
which  is  unknown,  in  the  cortical  part  of  the  central  neu- 
ron, by  which  an  impulse  is  liberated  and  caused  to  de- 
scend the  neuraxon.  Its  energy  is  then  transferred  by 
means  of  the  terminal  filaments  to  the  peripheral  neuron, 
along  which  it  passes  to  the  muscle  fiber,  which  it  stimulates 
and  causes  to  contract.  When  for  any  reason  the  creative 
power  of  the  cell  body  of  the  central  neuron  is  abolished, 
or  the  conductivity  of  its  lower  part  or  of  the  peripheral 
neuron  is  lost,  the  muscles  which  are  controlled  by  these  ele- 
ments can  not  receive  the  stimulus  necessary  for  their  con- 
traction, and  are  consequently  paralyzed. 

The  clinical  manifestations  of  paralysis  vary  according- 
as  the  lesion  exercises  its  inhibitory  or  destructive  action 
upon  the  central  or  the  peripheral  neuron. 

SYMPTOMS   OF  CENTRAL  NEURON       SYMPTOMS    OF   PERIPHERAL  NEU- 
INJURY.  RON    INJURY. 

Paralysis,  Paralysis, 

Rigidity,  Flaccidity, 

Increase  of  tendon  reflexes,  Loss  of  all  reflexes, 

Loss  of  peripheral  reflexes. 

Preservation    of    normal    elec-  Degenerative     electrical     reac- 

trical  reactions,  tions, 

Atrophy  slight  or  absent,  Atrophy  early  and  decided. 

Trophic  disturbances  not  promi-  Trophic     disturbances      promi- 
nent, nent. 

Exception  must  be  made  for  the  distinctive  character  of 
these  symptoms  in  so  far  as  that  after  acute  injuries  all  re- 
flexes may  be  absent  for  a  time  ;  paralysis  may  remain  fiaccid 
for  hours  or  days  ;  and  that  at  least  five  days  ai'e  necessary  for 
the  development  of  degenerative  electrical  reactions.     The 


c6  ORGANIC   EFFECTS   OF   INJURY. 

pure  type  of  central  neuron  paralysis  is  seen  only  in  injuries 
occurring  in  or  above  the  basal  ganglia  of  the  brain.  In 
these  situations  none  of  the  neuraxons  have  reached  their 
lowest  destination,  and  since  a  peripheral  neuron  does  not 
begin  until  its  central  neuron  ends,  there  are  no  peripheral 
neurons  in  the  vicinity  of  the  lesion,  and  the  paralysis  accord- 
ingly corresponds  to  the  central  neuron  type.  The  pons, 
medulla,  and  spinal  cord,  on  the  other  hand,  contain  such 
peripheral  neurons  as  are  making  their  exit  from  the  cere- 
bro-spinal  axis  (cranial  and  peripheral  nerves),  and  also  those 
central  neurons  which  are  still  descending  to  be  connected 
with  the  peripheral  neurons  which  are  situated  at  lower 
levels.  Consequently,  while  injuries  of  the  cerebrum  pre- 
sent symptoms  referable  to  lesions  of  the  central  neuron 
only,  those  at  the  base  of  the  brain  or  in  the  spinal  cord 
usually  give  evidence  of  interference  with  both  neurons. 
Thus  an  injury  to  one  side  of  the  pons,  in  a  situation  below 
the  crossing  of  the  facial  nerve,  causes  a  facial  palsy  on  the 
same  side  as  the  lesion  (peripheral  neuron),  while  the  paraly- 
sis of  the  arm  and  leg  is  on  the  other  side  of  the  body,  and 
of  central  neuron  type. 

In  addition  to  the  types  of  paralysis,  according  as  one 
or  the  other  neuron  is  affected,  there  are  certain  means  of 
localization  of  the  injury  afforded  by  associated  signs,  which 
are  present  when  the  lesion  is  in  some  situations  and  which 
are  absent  when  it  is  in  others. 

Cortical  injuries  commonly  cause  paralysis  of  the  arm 
and  leg,  less  frequently  of  the  arm,  leg,  and  face.  When 
the  cortex  is  injured,  convulsions  are  common,  as  is  seen  in 
traumatic  epilepsy  or  in  the  twitchings  of  muscles  recently 
paralyzed  ;  there  may  also  be  a  loss  of  the  sense  of  position 
and  some  disturbance  of  cutaneous  sensation.  Monoplegia 
rarely  results  from  traumatism  of  the  brain  ;  when  it  occurs 
it  is  due  to  a  selective  injury  to  the  cortex. 

In  the  tracts  below  the  cortex  smaller  lesions  cause  more 


INJURIES   TO   THE   BRAIN.  57 

extensive  paralysis,  as  in  those  situations  the  motor  fibers  are 
more  closely  packed  together  and  the  pathway  is  smaller. 

Lesions  of  the  internal  capsnle  cause  hemiplegia  of  the 
opposite  side;  when  situated  posteriorly,  there  may  also  be 
diminution  of  cutaneous  sensibility  and  hemianopsia.  Le- 
sions at  the  base  of  the  brain,  by  pressing  upon  or  destroy- 
ing the  neuraxons  of  those  central  neurons  which  preside 
over  voluntary  motion  in  the  limbs,  may  cause  paralysis  of 
them  of  various  distributions.  But  in  addition  to  the  pal- 
sies of  the  limbs,  central  neuron  type,  there  are  usually 
palsies  of  the  cranial  nerves,  peripheral  neuron  type. 

The  pons,  as  well  as  the  cortex,  contains  a  convulsive 
center,  and  consequently  lesions  at  the  base  of  the  brain, 
which  irritate  the  pontine  region,  are  followed  by  muscu- 
lar twitchings  or  by  general  convulsions.  Pontine  lesions 
also  usually  cause  ansesthesia. 

If  the  lesion  is  in  the  anterior  fossa  of  the  skull,  the  only 
cranial  nerves  affected  are  the  olfactory  and  optic. 

Symptoms  of  direct  injury  to  the  olfactory  ncj'ves  are 
rare.  They  consist  of  disturbances  of  smell,  which  are  usu- 
ally associated  with  impairment  of  taste.  Fractures  at  the 
base  of  the  skull  and  penetrating  wounds  not  uncommonly 
cause  laceration  or  hsemorrhage  into  the  sheaths  of  the 
optic  nerves.  If  either  optic  nerve  is  injured  in  front  of  the 
chiasm,  the  result  is  more  or  less  complete  blindness  in  the 
eye  of  the  same  side.  The  ophthalmoscope  shows  optic 
neuritis,  which  may  be  followed  by  atrophy. 

Injury  of  the  optic  nerve  at  the  chiasm  causes  bilateral 
blindness.  If  the  optic  tract  is  injured  posteriorly  to  the 
chiasm  the  result  is  hemianopsia.  Palsy  of  the  tJiird  nerve, 
either  total  or  in  some  of  its  fibers  only,  is  one  of  the  most 
frequent  evidences  of  injuries  in  the  vicinity  of  the  orbit  and 
at  the  base  of  the  brain.  From  the  controlling  influences 
which  this  nerve  exercises  upon  the  eyelid,  upon  most  of 
the  extrinsic  muscles  of  the  eyeball,  and  upon  the  size  of  the 


58 


ORGANIC  EFFECTS  OF  INJURY. 


Fig.  13.  —  Double  third  -  nerve 
palsy,  showing  outward  and 
downward  deviation  of  both 
eyes  and  wrinkling  of  the  fore- 
head.    (Incurable  Hospital.) 


pupil,  an  abolition  of  its  function  causes  striking  symptoms. 
When  the  nerve  is  the  seat  of  a  complete  lesion,  there  are 
ptosis,  outward  and  downward  rotation  of  the  eye  from  the 

overaction  of  the  external  rectus 
and  the  superior  oblique,  and  dil- 
atation of  the  pupil  (Fig.  13).  Com- 
plete third-nerve  palsy,  however,  is 
comparative!}^  rare  in  acute  condi- 
tions. More  frequently  the  nerve 
shows  a  partial  and  selective  palsy. 
Thus  there  may  be  a  drooping  of 
the  upper  lid,  so  that  the  affected 
eye  can  not  be  opened  as  wide  as 
the  normal  eye;  or  there  maybe 
only  a  slight  dilatation  of  the  pupil 
on  the  injured  side,  so  that  there 
exists  an  inequality  in  the  size  of  the  pupils,  the  larger  being 
on  the  side  of  the  injury ;  or  there  may  be  a  weakness  in  the 
extrinsic  muscles  supplied  by  the  third  nerve. 

Palsy  of  the  fourth  nerve  is  uncommon,  and  unless  pro- 
nounced is  only  demonstrable  by  means  of  prisms. 

The  fifth  nerve  usually  escapes  intracranial  lesion  and  is 
never  injured  alone  in  this  situation.  Its  affection  is  re- 
vealed by  palsy  of  the  masseters  and  buccinators  and  by 
angesthesia,  with  pain  over  the  face  and  forehead.  If  the 
fibers  to  the  eyeball  are  involved  there  results  neuropara- 
lytic ophthalmia. 

The  sixth  nerve  is  frequently  the  seat  of  traumatic  pa- 
ralysis. Through  the  resulting  weakness  of  the  external 
rectus,  the  eyeball  is  turned  inward  and  movements  out- 
ward are  limited  or  impossible.  Palsy  of  any  of  the  ocular 
nerves  causes  the  subjective  sensation  of  diplopia. 

Intracranial  facial  {seventh  7ierve)  paralysis  differs  from 
extracranial  facial  paralysis  in  that  there  may  be  added  dis- 
turbances of  taste  and  of  salivary  secretion.     When  of  trau- 


INJURIES   TO   THE    BRAIN. 


59 


matic  origin  it  is  invariably  unilateral  and  associated  with 
disturbances  of  the  auditory  7icrve,  such  as  deafness,  sub- 
jective auditory  sensations,  and  dizziness.  Palsy  of  the 
nerve  will  be  considered  more  fully  on  a  later  page.  By 
reason  of  their  situation,  the  glossopharyngeal,  pneumogas- 
tric,  and  hypoglossal  nerves  are  never  paralyzed  by  acute 
intracranial  injuries,  which  are  not  almost  immediately  fatal. 
Sometimes  several  cranial  nerves  are  paralyzed  together. 
A  characteristic  clinical  type  of  such  multiple  nerve  lesions, 


T"iG.  14. — Photograph  showing  paralysis  of 
the  left  sixth  and  seventh  nerves,  due  to 
a  fracture  of  the  skull.  Patient  trying 
to  look  straight  ahead. 


Fig.  15. — Same  case.  Patient  trying  to 
look  toward  the  left.  (Vanderbilt 
Clinic.) 


sometimes  seen  after  fractures  at  the  base,  is  illustrated  by 
the  following  case  (Figs.  14,  15). 

The  patient  came  to  the  Vanderbilt  clinic  complaining  of  deaf- 
ness, double  vision,  and  the  drawing  of  the  face  to  one  side.  He 
told  us  that  twelve  weeks  previously  he  fell  twelve  feet,  striking 
on  the  buttocks;  he  lost  consciousness  for  some  time,  and  on 
coming  to  himself  observed  the  symptoms  above  mentioned,  to- 
gether with  bleeding  from  the  left  ear.    Our  examination  showed: 


5o  ORGANIC   EFFECTS   OF   INJURY. 

partial  paralysis  of  left  external  rectus  (sixth  nerve),  peripheral  pa- 
ralysis of  left  side  of  face  (seventh  nerve),  deafness  in  left  ear  with 
loss  of  bone  conduction  (eighth  nerve).  The  appearance  of  the 
patient  was  highly  characteristic:  the  left  side  of  the  face  was 
flattened,  a  condition  which  was  caused  by  a  contraction  of  the 
muscles  of  the  right  side.  When  the  patient  looked  straight  in 
front  of  him  there  was  a  left  internal  squint  caused  by  overaction 
of  the  internal  rectus ;  when  he  tried  to  look  toward  the  left, 
the  right  eye  executed  the  movement  normally,  but  the  left 
looked  straight  ahead  from  inability  of  the  left  external  rectus 
to  rotate  the  eyeball  outward. 

However,  in  traumatic  affections  at  the  base  of  the  brain 
there  is  only  rarely  the  opportunity  for  that  accuracy  of 
topographical  diagnosis  which  is  so  generally  possible  in 
chronic  lesions.  The  former  result,  in  the  vast  majority  of 
cases,  from  fractures  at  the  base  of  the  skull  which  cause 
such  extensive  haemorrhages  or  lacerations  of  the  cranial 
nerves  or  of  the  cerebral  substance  that  it  is  usually  impos- 
sible to  determine  as  to  the  existence  of  discrete  multiple 
lesions,  and  the  physician  or  surgeon  generally  has  to  con- 
tent himself  with  making  the  diagnosis  of  injury  at  the  base 
of  the  brain,  without  definitely  ascertaining  its  exact  loca- 
tion. 

The  symptoms  of  injury  to  the  cerebellum  are  often  in- 
definate.  Lesion  of  the  lateral  lobes  gives  no  localizing  symp- 
toms. If  the  middle  lobe,  or  worm,  is  involved,  there  is  the 
characteristic  cerebellar  ataxia,  which  may  be  associated 
with  loss  of  knee-jerks.  Injuries  to  the  medulla  are  always 
immediately  fatal. 

Sensory  Symptoms. — Pronounced  ansesthesia  is  rarely 
if  ever  observed  as  a  focal  symptom  of  traumatisms  of  the 
brain. 

After  severe  injuries,  when  the  coma  is  profound,  there  is 
often  a  generalized  diminution  or  a  total  loss  of  cutaneous 
sensibility,  as  is  shown  by  the  patient's  indifference  to  the 
application  of  painful  stimuli.     But  this  is  to  be  interpreted 


INJURIES    TO    THE    BRAIN.  6 1 

as  a  disturbance  of  the  receptive  centers,  due  to  abolition  of 
mental  function,  rather  than  as  an  indication  of  any  interrup- 
tion of  conducting  paths.  This  assumption  receives  addi- 
tional proof  from  the  fact  that  sensibility  almost  invariably 
returns  with  a  restoration  to  consciousness.  If  there  is  a 
well  marked  hemiplegia,  complaints  of  subjective  sensations 
of  pricking  or  numbness  in  the  paralyzed  side  may  be  made, 
and  by  examination  with  the  needle  or  with  cotton  it  may 
become  evident  that  there  is  some  blunting  of  sensibility  on 
the  paralyzed  side.  But,  although  the  patient  does  not  feel 
so  well  on  that  side  as  on  the  other,  he  can  still  distinguish 
between  hot  and  cold,  can  tell  when  he  is  touched,  and 
gives  some  expressions  of  pain  upon  the  application  of 
painful  stimuli — evidences  of  hypassthesia  rather  than  of 
anaesthesia.  Hemihypsesthesia,  associated  with  disturbances 
of  the  sense  of  position,  is  a  not  infrequent  result  of  injuries 
of  the  motor  cortex. 

Lesions  which  result  from  external  violence  and  which 
affect  the  cerebral  sensory  tracts  probably  never  cause 
complete  hemianassthesia,  with  involvement  of  the  head, 
trunk,  and  extremities,  such  as  is  frequently  seen  in  hysteria. 
In  cortical  injuries  the  resulting  anaesthesia  is  never  total 
and  is  rarely  pronounced  in  degree.  Pressure  upon  the  pos- 
terior third  of  the  hinder  limb  of  the  internal  capsule  may 
bring  about  complete  loss  of  sensibility  to  all  stimuli  on  the 
opposite  side  of  the  body;  or  pressure  upon  the  pons  in  the 
neighborhood  of  the  fifth  nerve  may  cause  "  crossed  hemi- 
ansesthesia  " — i.  e.,  loss  of  sensibility  in  the  distribution  of 
the  fifth  nerve  on  the  side  of  the  lesion  and  anaesthesia  of 
the  arms,  trunk,  and  legs  of  the  opposite  side.  Cases  pre- 
senting these  symptoms  have  been  reported,  but,  as  far  as  I 
know,  they  have  been  the  results  of  tumors  or  of  non-trau- 
matic vascular  disturbances  exclusively.  It  can  not  be  de- 
nied, however,  that  similar  symptoms  might  result  from  lac- 
eration of  the  brain,  or  from  haemorrhages  into  it,   which 


62  ORGANIC   EFFECTS   OF    INJURY. 

were  caused  by  quickly  acting  external  violence,  but  if  such 
a  possibility  exists,  evidence  in  its  favor  has  escaped  my 
notice  ;  and,  indeed,  it  seems  hardly  probable  that  any  trau- 
matism could  act  in  a  way  to  produce  so  small  and  so  selec- 
tive a  lesion  as  would  be  necessary  to  cause  the  pure  type 
of  hemianaesthesia,  such  as  is  produced  by  interference  with 
the  sensory  tracts  in  the  pons  or  in  the  internal  capsule, 
without  at  the  same  time  so  seriously  injuring  other  parts 
of  the  brain  that  the  unilateral  character  of  the  sensory  loss 
was  not  maintained,  or  that  the  sensory  symptoms  became 
masked  by  more  serious  nervous  disturbances. 

As  will  be  mentioned  in  succeeding  pages,  hemianses- 
thesia — profound,  total,  and  sharply  limited  by  the  median 
line  of  the  body — is  not  uncommonly  observed  in  the  victims 
of  railway  and  allied  disasters.  To  it  Charcot  ascribed  a 
pathognomonic  value  in  the  diagnosis  of  hysteria,  a  view 
which  was  opposed  in  Germany.  Without  entering  here  ''' 
into  further  discussion  of  the  question,  it  may  be  safely 
asserted  that  when  pronounced  hemiancesthesia  appears  as 
one  of  the  clinical  results  of  an  accident  it  is  in  all  proba- 
bility hysterical,  and  that  if  this  symptom  is  ever  the  result 
of  an  organic  injury  to  the  brain,  the  inevitable  association 
of  other  symptoms  of  cerebral  lesion  will  leave  no  doubt  as 
to  its  nature  and  origin. 

Reflexes. — As  a  rule,  after  injuries  to  the  head  which 
have  been  severe  enough  to  cause  profound  coma,  both  the 
skin  and  tendon  reflexes  are  temporarily  lost.  The  general 
absence  of  reflexes  indicates  that  the  brain  has  been  seri- 
ously injured,  but  gives  no  indication  as  to  the  seat  or  the 
character  of  the  lesion. 

When  the  initial  coma  is  less  profound,  or  when  it  is 
beginning  to  pass  away,  the  condition  of  the  reflexes  is 
capable  of  furnishing  more  definite  information. 

All  the  reflexes  on  the  paralyzed  side  may  be  absent, 
while  those  of  the  unaffected  side  remain  about  normal,  or 


VARIETIES   OF   BRAIN   INJURIES.  63 

— and  especially  if  the  examination  is  made  a  few  days  after 
the  accident — there  may  be  a  unilateral  increase  of  tendon 
reflex  activity  on  the  side  of  the  paralysis,  while  the  abdomi- 
nal reflexes  of  that  side  remain  unelicitable.  The  unilateral 
absence  of  abdominal  reflexes,  with  increase  in  the  knee-  or 
wrist-jerk,  is  one  of  the  most  valuable  diagnostic  signs  of 
hemiplegia,  and  may  be  present  when  the  loss  of  motor 
power  is  very  slight. 

Bladder  and  Rectum. —  In  deep  coma  there  may  be  the 
retention  of  urine,  or  the  involuntary  passage  of  urinary 
and  feecal  discharges,  which  is  the  rule.  When  the  patient 
is  conscious  there  is  usually  no  loss  of  control  of  the  blad- 
der or  rectum  as  a  result  of  cerebral  injuries. 

Varieties  of  Brain  Injuries. 

The  brain  is  very  much  less  securely  protected  against 
injury  than  the  spinal  cord,  there  being  wanting  the  thick 
cushions  of  muscles,  and  the  bones  which  surround  the 
encephalon  being  thinner  and  less  resistant  than  those  which 
inclose  the  spinal  cord.  A  blow  which,  if  applied  to  the 
back,  would  be  followed  by  no  evidences  of  spinal  cord 
lesion,  might,  if  applied  to  the  head,  cause  serious  cerebral 
injuries.  By  blows  on  the  head,  by  falls,  or  by  the  entrance 
of  foreign  bodies,  the  skull  may  be  fractured  and  the  brain 
be  contused  or  lacerated,  either  directly  by  splinters  of 
bone  or  indirectly  by  transmitted  force.  Haemorrhage  may 
occur  from  vessels  which  are  ruptured,  either  in  the  bone, 
in  the  membranes,  or  in  the  brain  substance,  or  there  may 
be  generalized  oedema  or  circumscribed  oedema  which  latter 
gives  focal  symptoms. 

Without  fracture  of  the  skull  the  intracranial  blood- 
vessels may  be  ruptured,  or  the  brain  substance  or  cranial 
nerves  may  be  contused  or  lacerated.  While  in  the  major- 
ity of  cases  the  skull  is  fractured,  the  fracture  is  often  not 
recognizable  during  life,  and   the  diagnosis  of  the  nature 


64  ORGANIC   EFFECTS   OF    INJURY. 

of  the  injury  must   be   made  from   the  nervous   symptoms 
alone. 

Concussion. — In  the  chapter  on  injuries  to  the  spinal 
cord  it  will  be  stated  that  there  is  still  much  doubt  as  to  the 
existence  of  any  such  condition  as  concussion  of  that  or- 
gan. The  probability  that  head  injuries  may  be  followed 
by  pronounced  cerebral  symptoms  without  there  being  any 
discernible  lesions  in  the  brain  is  very  much  stronger. 
There  is,  of  course,  no  question  but  that  after  many  head 
injuries  multiple  hemorrhages  occur,  especially  in  the  gray 
matter,  which  do  not  give  any  localizing  symptoms,  and 
that  in  many  of  these  cases  the  condition  must  be  diagnos- 
ticated clinically  as  that  of  cerebral  concussion.  But  the 
results  of  daily  clinical  experience  leave  hardly  room  for 
doubt  that,  after  very  insignificant  head  injuries,  there  occur 
unconsciousness  and  other  slight  cerebral  symptoms  of  too 
trivial  a  character  to  be  dependent  upon  any  lesion  so  gross 
as  hasmorrhage.  To  cite  an  example  familiar  to  boxers,  a 
blow  on  the  point  of  the  jaw  may  deprive  the  victim  of  all 
appreciation  of  his  surroundings.  Yet  in  a  few  moments  he 
is  entirely  recovered  and  ready  to  continue  the  fray.  He 
has  suffered  temporarily  from  cerebral  concussion.  From 
these  conditions,  when  the  patient  is  for  a  few  minutes 
without  consciousness,  to  those  in  which  he  lies  for  da^-s 
in  coma,  stupor,  or  delirium,  there  are  various  intermediate 
stages ;  and  while,  in  the  severer  cases,  we  may  suspect  dur- 
ing life  and  be  able  to  prove  after  death  that  the  symptoms 
depended  upon  multiple  though  minute  hjemorrhages  and 
lacerations,  there  are  many  patients  who  do  not  die,  and 
who,  by  the  speediness  of  their  recovery,  indicate  that  the 
brain  has  received  no  severe  injury.  In  the  absence  of  local- 
izing signs  we  are  unable  to  distinguish  between  the  differ- 
ent varieties  of  cerebral  concussion,  and  we  are  consequently 
obliged  to  designate  by  the  same  term  conditions  which 
may  be  very  different. 


VARIETIES   OF    BRAIN    INJURIES.  65 

The  symptoms  of  cerebral  concussion  may  be  slight  or 
severe.  In  consideration  of  the  fact  that  serious  organic 
injuries  of  the  brain  may  for  a  long  time  cause  no  pro- 
nounced cerebral  symptoms,  the  physician  can  hardly  be 
accused  of  overcautiousness  if  he  refuses  to  diagnosticate 
cerebral  concussion  until  the  patient  has  been  under  obser- 
vation for  several  days. 

After  the  injury  there  may  be  deep  coma  or  stupor,  or 
only  mental  confusion.  Delirium  is  not  infrequent,  and  in 
alcoholic  patients  its  occurrence,  associated  with  zooscopic 
hallucinations,  is  the  rule. 

The  patient  may  be  induced  to  answer  questions,  but  his 
mind  immediately  wanders  again;  he  may  seem  partially 
conscious  and  yet  not  recognize  his  surroundings.  The 
memory  of  the  accident  is  often  entirely  lost.  There  is 
usually  headache,  which  may  be  very  intense,  and  associ- 
ated with  intolerance  of  light  and  sound.  Dizziness,  nausea, 
vomiting,  and  convulsions  are  frequent  symptoms.  The 
pulse  is  slow  and  regular,  and  the  breathing  is  superficial. 
The  tendon  reflexes  are  exaggerated,  especially  in  severe 
cases. 

With  the  exception  of  nystagmus  and  alternating  strabis- 
mus there  are  no  focal  signs.  As  soon  as  any  localizing 
signs  appear,  such  as  unilateral  increase  of  reflexes,  or  pa- 
ralysis of  the  limbs,  or  evidences  of  injury  to  the  cranial 
nerves,  the  diagnosis  of  concussion  must  be  changed  to  that 
of  a  more  definite  lesion.  Consequently  the  diagnosis  is  one 
by  exclusion. ,  Cerebral  concussion  is  an  accompaniment  of 
all  severe  brain  injuries,  but  under  such  circumstances  its 
symptoms  are  masked  by  those  of  the  graver  conditions. 

The  duration  of  the  condition  depends  on  its  severity. 
Usually  the  patient  is  able  to  get  up  in  the  course  of  a  few 
days,  although  there  may  be  left  evidences  of  mental  impair- 
ment which  are  a  long  time  in  disappearing,  or  which  may 
not  disappear  at  all. 


65  ORGANIC   EFFECTS   OF    INJURY. 

Fractures. — In  fractures  of  the  cranial  vault  there  are 
often  external  evidences  of  the  condition,  such  as  depres- 
sions or  fissures  in  the  bones.  These  may  be  wanting, 
however,  and  in  fractures  at  the  base  they  are  never  pres- 
ent, so  that  the  diagnosis  must  be  made  from  the  nervous 
symptoms  alone,  or  from  such  signs  of  leakage  as  subcon- 
junctival ecchymosis  or  discharges  from  the  ears  or  nose. 

When  persons  are  found  unconscious,  with  paralytic 
symptoms,  with  or  without  scalp  wounds,  it  is  not  always 
easy  to  determine  whether  the  coma  is  apoplectic  in  origin, 
or  whether  it  is  a  result  of  a  fracture  of  the  skull. 

In  the  summer  of  1896  one  of  the  feniale  inmates  of  the  Work- 
house, aged  sixty,  was  found  on  the  floor  of  her  cell  unconscious, 
presumably  having  fallen  from  her  bunk  to  the  stone  floor,  a  dis- 
tance of  about  four  feet.  There  was  a  deep  scalp  wound  over  the 
left  parietal  eminence.  She  was  transferred  to  the  hospital,  and 
when  I  saw  her  she  was  m  partial  coma,  with  a  right  hemiplegia 
unassociated  with  aphasia.  The  question  was.  Did  the  patient 
fall  and  receive  a  scalp  wound  as  the  result  of  an  apoplectic  at- 
tack, or  was  her  condition  due  to  a  fracture  of  the  skull,  with 
resulting  injury,  or  compression  of  the  brain  ?  There  were  no 
external  evidences  of  fracture.  There  were  no  palsies  of  the 
cranial  nerves,  except  that  the  right  pupil  was  larger  than  the 
left.  The  hemiplegia,  which  was  complete,  involved  the  arm,  leg, 
and  face;  there  were  no  convulsions,  and  only  slight  disturb- 
ances of  sensation.  All  these  symptoms  indicated  with  proba- 
bility, but  not  with  certainty,  a  primary  cerebral  haemorrhage 
rather  than  a  laceration  or  traumatic  compression  of  the  brain. 
The  autopsy,  held  ten  days  after  the  accident,  confirmed  this 
opinion.  There  was  a  large  haemorrhage  in  the  left  internal  cap- 
sule, but  no  injury  to  the  other  parts  of  the  brain,  and  no  fracture 
of  the  skull. 

In  such  cases  the  absence  of  all  external  signs  of  fracture, 
the  complete  hemiplegia  without  involvement  of  the  cranial 
nerves,  and  the  occurrence  at  a  pei-iod  of  life  when  apoplecti- 
form attacks  are  common,  are  suggestive  of  primary  rather 
than  traumatic  brain  lesion.  But  the  diagnosis  is  always 
difficult,  and  in  many  cases  can  not  with  certainty  be  made. 


VARIETIES   OF    BRAIN    INJURIES.  67 

There  is  no  domain  in  medicine  or  surgery  in  which 
more  caution  in  diagnosis  and  prognosis  is  required  than 
in  head  injuries. 

In  fractures  of  the  skull  the  patient  may  present  no 
evidences  other  than  those  of  concussion  for  days  or  weeks, 
and  then  suddenly  develops  symptoms  of  an  alarming  or 
fatal  character.  It  is  a  common  occurrence  for  persons 
whose  skulls  are  fractured  to  walk  to  hospitals  or  to  be 
arrested  for  disorderly  conduct  on  the  street. 

In  a  case  communicated  to  me  by  Dr.  Psotta,  House  Surgeon 
of  Roosevelt  Hospital,  a  man  fell  off  a  cable  car,  was  rendered 
unconscious,  and  was  brought  to  the  hospital.  There  were  no 
evidences  discoverable  of  fracture  of  the  skull  or  of  local  brain  in- 
jury, and  the  next  day,  as  the  patient  was  feeling  perfectly  well, 
he  was  discharged  from  the  hospital.  He  continued  to  feel  well 
for  two  weeks,  when  he  suddenly  died.  An  autopsy  by  the  coroner 
showed  a  fracture  running  transversely  for  the  whole  width  of 
the  middle  fossa  of  the  skull. 

The  most  that  the  physician  or  surgeon  can  do  in  these 
difficult  cases  is  to  ascertain,  as  nearly  as  possible,  the  se- 
verity of  the  accident,  and,  after  severe  accidents,  to  with- 
hold an  opinion  until  sufficient  time  has  elapsed  to  render 
the  occurrence  of  further  symptoms  improbable. 

Any  head  injury  is  liable  to  be  complicated  by  intracra- 
nial inflammation,  and  the  symptoms  of  meningitis,  abscess, 
or  encephalitis  may  be  added  to  those  of  conditions  which 
did  not  at  first  seem  serious. 


CHAPTER   11. 

Injuries  to  the  Spinal  Cord. 

Although  the  studies  of  recent  years  have  cleared 
away  much  of  the  confusion  with  which  the  writings  of 
Erichsen  enshrouded  spinal-cord  injuries,  the  terminology 
applied  to  these  affections  to-day  is  far  from  satisfactory. 
For  this  the  unfortunate  survival  of  the  expression  "  con- 
cussion of  the  spinal  cord  "  is  largely  responsible. 

As  used  to-day,  this  term  is  extremely  indefinite  in  its 
meaning.  There  is,  of  course,  no  longer  excuse  for  apply- 
ing it  to  the  forms  of  nervous  disease  which  are  purely 
functional  in  character  (traumatic  neurasthenia),  nor  to  the 
cases  in  which  there  may  be  slight  injuries  to  the  verte- 
bral joints  without  affection  of  the  more  delicate  structures 
beneath  them  (lumbago).  But  aside  from  its  use,  or  misuse, 
as  applying  to  affections  in  which  there  is  no  disturbance 
of  the  structure  of  the  spinal  cord  itself,  it  remains  as 
a  designation  of  lesions  for  which  the  names  myelitis, 
softening,  and  haemorrhage  are  alone  permissible.  Some 
writers  call  any  injury  to  the  spinal  cord  "  spinal  concus- 
sion "  ;  others  use  the  term  for  any  spinal  affection  which 
may  result  from  concussion  accidents ;  still  others  make  it 
synonymous  with  intraspinal  haemorrhage,  with  or  without 
vertebral  lesion.  A  conservative  few  restrict  it  to  those 
cases  in  which,  with  absence  of  injury  to  the  spinal  column, 
there  may  be  evidences  of  focal  injury  to  the  spinal  cord 
which  has  not  been  caused  by  haemorrhage. 

Since  it  is  still  a  matter  of  doubt  that  there  exists  any 


INJURIES   TO   THE    SPINAL   CORD.  69 

pathological  condition  such  as  the  term  spinal  concussion 
in  its  most  restricted  sense  would  imply,  to  retain  so  gen- 
erally familiar  a  designation  for  a  condition  which,  if  it 
exists  at  all,  is  extremely  rare,  will  certainly  prove  an 
obstacle  to  the  advancement  of  our  knowledge  of  the 
causal  relations  of  traumatism  to  spinal  disease.  It  is,  how- 
ever, much  easier  to  object  to  than  to  do  away  with  a  term 
which  has  gained  popularity.  I  would  nevertheless  strongly 
urge  that  if  "  concussion  of  the  spinal  cord  "  is  to  be  re- 
tained at  all  in  medical  nomenclature,  it  should  be  re- 
stricted to  those  cases  in  which  it  can  be  shown  that  the 
nervous  elements  of  the  cord  have  been  directly  injured, 
without  having  been  compressed  by  bone  or  by  extrava- 
sated  blood. 

The  degree  of  violence  necessary  to  cause  injury,  either 
directly  or  indirectly,  to  the  spinal  cord  is  very  great.  No 
organ  in  the  body  is  so  strongly  secured  against  danger. 
It  is  held  in  place  above  and  below  by  attachments  of  the 
dura  mater,  and  at  the  sides  by  its  thirty-one  pairs  of  nerves. 
Between  the  two  membranes  which  surround  it  is  a  thick 
column  of  fluid  that  envelops  it  in  its  whole  extent,  and 
which  acts  as  a  cushion  in  dissipating  the  force  of  any 
shocks  which  may  be  received  by  the  spine.  The  vertebrae 
(Fig.  16)  through  which  it  passes  are  thick  and  strong,  are 
held  in  place  by  tough  ligaments,  and  are  everywhere 
padded  by  massive  layers  of  muscles. 

The  accuracy  and  compactness  of  the  articulation  of  its 
parts  enable  the  spinal  column  to  withstand  great  degrees 
of  strain  and  force  before  its  own  integrity  or  that  of  the 
spinal  cord  is  disturbed.  Yet,  notwithstanding  the  solid 
strength  of  the  vertebrae,  their  nicety  of  adjustment,  the 
massed  layers  of  muscles,  and  its  other  efficient  means  of 
protection,  the  spinal  cord  is  not  infrequently  the  seat  of 
serious  injuries.  But  the  injuries  which  overcome  the 
barriers  by  which  it  is  shielded  from  danger  are  the  results 


70 


ORGANIC  EFFECTS  OF  INJURY. 


of   excessive    violence   that  acts   directly  upon    the   spinal 
column. 

Thus  from  severe  falls  or  blows  upon  the  head   there 
may  result  spinal-cord  injury,  even  though  the  skull  escapes 


Fig.  t6. — Transverse  section  of  the  structures  surrounding  the  spinal  cord 
at  the  line  of  the  ninth  thoracic  vertebra 

fracture.  Falls  on  the  buttocks,  either  from  heights  or, 
as  occasionally  occur  in  consequence  of  elevator  accidents, 
may  produce  a  like  result.  Penetrating  wounds,  or  blows 
on  the  back  from  heavy  objects,  may  be  immediately  fol- 
lowed by  symptoms  of  impairment  or  loss  of  spinal  func- 
tion. By  very  severe  and  sudden  twists  or  wrenches  it  is 
possible  for  vertebrge  to  be  dislocated  or  for  some  of  the 
intravertebral    structures    to    be    torn.      But    the    violence 


INJURIES   TO   THE    SPINAL   CORD.  yi 

which  causes  these  injuries  is  extreme,  and  differs  both  in 
character  and  in  degree  from  such  violence  as  may  be  re- 
ceived by  the  sudden  stopping-  or  starting  of  a  train,  or  from 
slipping  on  a  banana  peel,  which  is  not  infrequently  ad- 
vanced as  a  cause  of  "  spinal  "  injury. 

It  is  obviously  difficult  to  determine  the  degree  of  force 
which  has  been  exerted  on  the  spinal  column  in  any  given 
accident.  Yet,  to  prove  the  existence  of  an  injury  to  the 
spinal  cord,  it  is  necessary  to  show  that  the  force  has  in  all 
probability  been  sufficient  to  break  through  the  vertebrae 
or  to  cause  stretching  or  laceration  of  the  structures  which 
they  surround.  Such  proof  is  established  when  the  symp- 
toms are  in  accord  with  those  we  now  recognize  as  indica- 
tive of  lesion  of  the  spinal  cord. 

Although  it  is  almost  always  possible  to  determine 
whether  the  spinal  cord  has  or  has  not  been  injured,  the 
diagnosis  of  the  exact  character  of  the  lesion  is  more  dif- 
ficult. That  our  knowledge  of  this  subject  might  be  very 
materially  advanced  by  the  careful  observation  of  a  large 
number  of  accident  cases  in  accordance  with  some  definite 
classification,  seems  reasonable  to  expect ;  and  for  the  fur- 
therance of  that  object  the  following  classification  is  pro- 
posed : 

I.  Spinal  column  injured,  by  wounds,  fractures,  and  dis- 
locations which  cause  compression  of  the  spinal  cord,  and, 
secondarily,  myelitis,  softening,  or  haemorrhage. 

II.  Spinal  column  uninjured,  but  spinal  cord  the  seat  of: 
I.  Compression  by  blood  clots.  2.  Ha3morrhage  into  cord 
substance.     3.  Concussion  or  commotion. 

The  clinical  applicability  of  such  a  classification  is,  of 
course,  in  the  present  state  of  our  knowledge,  restricted, 
since  where  there  are  no  external  evidences  of  vertebral 
injury  it  is  usually  impossible  to  be  certain  of  the  exact 
character  of  the  cord  lesion.  From  the  standpoint  of  patho- 
logical anatomy,  however,  it  is  justifiable,  and  it  seems  not 


72 


ORGANIC    EFFECTS   OF    INJURY. 


unreasonable  to  hope  that  pathological  studies  conducted 
along  its  lines,  when  preceded  by  accurate  clinical  observa- 
tions, would  so  much  enlarge  our  comprehension  of  the 
nature  of  spinal-cord  injuries  that  they  could  be  accurately 
diagnosticated  during  the  life  of  the  patient.  In  accordance 
with  this  classification  injuries  to  the  spinal  cord  will  now  be 
briefly  discussed. 

I.  Spinal  Column  Injured. 

By  far  the  larger  number  of  traumatic  lesions  of  the 
spinal  cord  are  secondary  to  injuries  of  the  vertebrae.  It 
is  often  impossible  to  determine  dur- 
ing the  life  of  the  patient  whether 
fracture  or  dislocation  of  the  bones 
has  or  has  not  occurred,  because  the 
integrity  of  the  spinal  column  may 
be  seriously  impaired  without  there 
being  any  irregularity  or  abnormal 
mobility  of  the  vertebral  spines.  Ex- 
ternal evidences  of  injury  are  absent 
with  particular  frequency  in  fractures 
which  involve  the  bodies  of  the  ver- 
tebrae only,  or  in  the  dislocations  re- 
sulting from  sudden  twists  or  wrench- 
es, in  which  the  bone  or  intervertebral 
cartilage,  after  having  been  momen- 
iiarily  thrust  forward  so  as  to  crush 
the  spinal  cord,  immediately  springs 
back  again  into  its  place  without  leav- 
ing external  traces  of  any  change  of 
position. 

Vertebral  lesions  may  cause  dam- 
age to  the  spinal  cord  in  a  variety  of  ways.  The  cord 
itself  may  be  cut  in  two  or  lacerated  or  crushed  (Fig.  17) 
by  dislocated  bone  or  by  splinters  of  bone ;  it  may  be  com- 


FiG.  17. — Crush  of  the  spi- 
nal cord,  due  to  fracture 
of  the  cervical  vertebrae. 
(From  a  drawing  kindly 
furnished  by  Dr.  Van 
Gieson.) 


SPINAL   COLUMN    INJURED. 


73 


pressed  by  haemorrhage  into  the  spinal  canal,  coming  from 
the  bone,  or  from  the  ligaments,  or  from  the  membranes 
(hsematorrhachis)  (Figs.  i8 
and  19);  its  blood-vessels 
may  be  so  torn  that  blood 
is  poured  out  into  the  cord 
tissue  itself  (hsematomyelia). 
From  any  of  these  lesions 
may  immediately  result  soft- 
ening or  inflammation  (mye- 
litis), or,  secondarily,  degen- 
erations or  gliosis  of  varying 
degrees.  The  symptoms  of 
any  of  these  conditions  indi- 


FlG.  18.— Intradural  hsemorrhage.  (From 
a  specimen  kindly  furnished  by  Dr.  G. 
E.  Brewer.) 


Fig.  19. — Extradural  haemorrhage. 
(Roosevelt  Hospital.; 


cate  a  focal  injury  to  the  spinal  cord,  and  will  be  described 
on  page  90. 

When  the  medullary  lesion  is   secondary  to  injuries  to 
the  bones  it  is  usually  impossible  to  decide  during  the  life 


74 


ORGANIC  EFFECTS  OF  INJURY. 


Fig.  20. — Diagram  to  illus- 
trate the  course  of  the  blood 
in  a  case  of  hasmatomyelia. 


of  the  patient  the  exact  nature  of 
the  pathological  condition  within 
the  spinal  canal.  In  such  cases  the 
cord  is  so  seriously  crushed  or  com- 
pressed at  the  seat  of  the  fracture 
that  the  symptoms  are  simply  those 
of  a  transverse  lesion,  whatever  tKe 
underlying  conditions  may  be. 

In  view,  however,  of  the  special 
pathological  interest  which  attaches 
to  hsematomyelia  the  following  case 
may  be  briefly  related  here.  Al- 
though the  lesion  was  too  extensive 
to  permit  any  inferences  as  to  the 
special  symptoms  of  central  haemor- 
rhage, the  disposition  of  the  blood 
was  characteristic  of  that  condition  : 

A  man  fell  on  his  head,  fracturing  the 
cervical  vertebrae.  He  did  not  lose  con- 
sciousness, but  was  immediately  para- 
lyzed in  all  four  extremities,  and  died  in 
a  few  days.  I  performed  the  autopsy  at 
the  City  Hospital  twelve  hours  after 
death.  Brain,  normal  ;  spinal  column, 
comminuted  fracture  of  the  third  and 
fourth  cervical  vertebrae.  On  opening 
the  dura,  the  outline  of  the  spinal  cord 
was  found  to  be  well  preserved,  though 
there  was  some  tendency  to  bulging  at 
the  fifth  and  sixth  cervical  segments. 
On  section  (Fig.  20)  there  was  a  sharply 
defined  haemorrhage  which  followed,  as 
nearly  as  the  naked  eye  could  see,  the 
gray  matter  of  these  two  segments.  Far- 
ther up  and  down  the  cord  there  was  a 
different  disposition  of  the  haemorrhage. 
The  blood  had  ascended  the  posterior 
horn    on    the    right    side   as   far  as  the 


SPINAL   COLUMN    INJURED.  ye 

middle  part  of  the  third  cervical  segment.  The  path  of  the  de- 
scending blood  followed  the  left  posterior  horn  of  the  cord  to  the 
lower  part  of  the  seventh  cervical  segment  (Fig.  21).  Studied  in 
microscopic  sections,  the  whole  of  the  fifth  and  sixth  cervical 
segments,  with  adjacent  portions  of  the  seventh  and  fourth,  were 
found  to  be  in  a  condition  of  acute  myelitis  with  its  ordinary 
appearances — viz.,  destruction  of  nerve  elements  with  a  cellular 
exudate  consisting  of  leucocytes  and  large  granular  cells.  In 
these  two  segments  the  blood-vessels  were  unusually  prominent 


Fig.  21. — Showing  inferior  termination  of  the  posterior  column  of  blood  in 
a  case  of  traumatic  hamatomyelia.     (City  Hospital.) 

and  dilated,  while  at  the  same  time  there  were  many  free  red  blood 
cells.  By  far  the  larger  number  of  the  red  blood  cells  were  col- 
lected in  the  gray  matter,  so  that  the  outlines  of  the  anterior  and 
posterior  horns  and  the  gray  commissure  were  brought  out  in 
sharp  relief.  In  the  other  segments  the  red  blood  cells  were  still 
more  closely  confined  to  the  gray  matter,  though  they  could  be 
seen  as  scattered  cells  throughout  all  the  sections.  With  the 
exception  of  the  fifth  and  sixth  segments,  there  was  little  inflam- 
mation or  softening,  and  the  nerve  fibers  were  well  preserved. 

The  amount  of  extravasated  blood  in  this  case  being  so  large, 
it  seems  probable,  although  it  can  not  be  positively  asserted,  that 
the  haemorrhage   resulted   directly  from   the  injury,  rather  than 


^6  ORGANIC  EFFECTS  OF  INJURY. 

that  it  was  secondary  to  the  softening  and  inflammation  by  which 
it  had  been  surrounded. 

II.  Spinal  Column  Uninjured, 

The  cases  in  which  the  spinal  cord  is  injured  while  the 
vertebral  column  remains  intact  form  only  a  small  propor- 
tion of  the  total  number  of  injuries  to  the  spinal  cord.  It 
is  consequently  in  regard  to  them  that  satisfactory  informa- 
tion is  difficult  to  obtain  and  that  our  knowledge  is  most 
incomplete.  Furthermore,  as  these  cases  are  naturally  less 
dangerous  to  life  than  the  ones  in  which  the  cord  lesions  are 
secondary  to  bone  lesions,  many  of  the  patients  recover  more 
or  less  completely,  and  the  nature  of  the  affection  remains 
largely  conjectural.  They  result  from  the  same  kind  of  vio- 
lence as  is  active  in  causing  fracture  and  dislocation  of  the 
spinal  column.  In  most  of  the  recorded  cases  of  this  variety 
of  injury  which  have  come  to  autopsy  the  lesion  has  con- 
sisted of  hsemorrhage. 

If  hemorrhage  is  the  chief  pathological  factor,  its  occur- 
rence may  be  explained  by  assuming  that  the  physical  shock 
was  sufficient  to  cause  a  rupture  of  some  of  the  blood-vessels 
of  the  spinal  membranes  or  of  the  spinal  cord.  Haemor- 
rhage may  occur  without  bone  lesion  (i)  within  the  spinal 
canal,  so  that  the  cord  is  compressed  by  blood  clots  (hasmat- 
orrhachis),  or  (2)  into  the  substance  of  the  cord  (hasmato- 
myelia).  Concussion  or  commotion  will  be  discussed  after 
these  hsemorrhagic  conditions. 

I.  HcBjnatorrhachis  may  be  illustrated  by  the  following 
case,  reported  by  Lambret : 

A  driver  fell  from  a  cart,  striking  on  his  head.  He  immedi- 
ately developed  symptoms  of  flaccid  paraplegia,  with  anaesthesia 
and  loss  of  sphincter  control,  and  as  a  result  of  his  injuries  died 
in  a  little  more  than  twenty-four  hours  after  the  accident.  At  the 
autopsy  both  skull  and  spinal  column  were  found  to  be  intact,  but 
there  was  a  long  extradural  blood  clot  in  the  spinal  canal  which 
had  compressed  the  spinal  cord  in  the  upper  dorsal  region. 


SPINAL   COLUMN    UNINJURED.  -j-j 

2.  Hcematoinyelia  (hccmorrhage  into  the  spinal  cord)  is 
one  of  the  most  interesting-  of  the  present  problems  of  the 
pathology  of  the  nervous  system.  Although  it  may  occur 
either  with  or  without  fracture  of  the  vertebrae,  its  chief 
clinical  interest  centers  about  the  cases  in  which  the  spinal 
column  remains  intact,  so  that  the  hcemorrhage  takes  place 
independently  of  crushes  of  the  cord.  In  hospitals  and,  less 
commonly,  in  clinics,  cases  are  met  with,  ninety  per  cent  of 
which  are  traumatic,  in  which  the  symptoms,  by  the  sud- 
denness of  their  onset  and  by  their  distribution,  point  to  the 
existence  of  this  condition.  Many  of  the  patients  recover 
more  or  less  completely,  so  that  the  diagnosis  remains 
unsubstantiated  by  post-mortem  demonstration.  In  others, 
death  ensues  so  rapidly  that  pathological  examination,  al- 
though showing  the  anatomical  condition,  leaves  undeter- 
mined what  the  ultimate  clinical  effects  would  have  been 
had  the  patient  lived. 

There  is  considerable  anatomical  evidence,  which  is 
based  upon  the  course  which  extravasated  blood  follows  in 
the  spinal  cord,  in  favor  of  the  view  that  central  haemor- 
rhage, if  not  too  extensive,  may  cause  symptoms  different 
from  those  of  a  transverse  lesion.  The  gray  matter  is  the 
least  resisting  portion,  and  its  vessels  are  the  most  liable 
to  rupture  ;  consequently,  in  many  of  the  cases  of  primary 
hgematomyelia,  the  hasmorrhage  occurs  in  and  remains  local- 
ized to  the  gray  matter,  although  it  may  burrow  for  long 
distances  up  and  down  the  cord. 

The  anatomical  condition  is  shown  by  a  case  of  Thor- 
burn's,  almost  identical  with  the  one  already  described,  ex- 
cept that  the  haemorrhage  occurred  independently  of  any 
fracture  of  the  spine. 

A  man  received  a  severe  blow  between  the  shoulders  and  be- 
came paralyzed  in  the  muscles  of  the  leg  and  abdomen  and  in  the 
intercostal  muscles.  After  three  days  of  the  ordinary  symptoms 
of  severe  spinal-cord  injury  he  died  with  congestion  of  the  lungs. 


y8  ORGANIC   EFFECTS   OF   INJURY. 

At  the  autopsy,  "in  the  muscles  over  the  lower  cervical  and  upper 
dorsal  regions  was  some  dark  effused  blood,  but  the  vertebral 
column  presented  no  evidences  of  injury.  The  membranes  of  the 
cord  were  quite  normal,  as  was  the  external  appearance  of  the 
cord  itself,  but  on  section  there  was  found  to  be  a  dark,  black 
haemorrhage  into  the  central  gray  matter  in  the  lower  cervical  and 
upper  dorsal  regions.  This  haemorrhage,  which  measured  in  its 
vertical  extent  from  one  and  a  half  to  two  inches,  was,  in  the 
greater  part  of  its  extent,  situated  centrally,  occupying  the  whole 
of  the  central  gray  matter  and  extending  but  little  into  the  white 
substance,  which  in  its  neighborhood  was  merely  softened  and  of 
a  faintly  yellow  tinge.  At  the  lower  part,  for  a  very  short  dis- 
tance, the  haemorrhage  was  limited  to  the  anterior  cornu  of  the 
right  side,  while  the  corresponding  left  horn  appeared  to  be  per- 
fectly healthy ;  elsewhere  the  cord  was  firm,  and  presented  no 
abnormity." 

In  cases  in  which  the  patients  have  partially  recovered, 
the  blood  extravasation  has  been  absorbed,  leaving-  long 
cavities  in  the  spinal  cord.  To  such  cavities  Levier  gave 
the  name  of  ''Rohrenbildung'' ;  in  an  elaborate  study  of  this 
condition,  as  yet  unpublished,  Van  Gieson  has  individualized 
the  sequelae  of  hasmatomyelia  under  the  term  "  hcematomye- 
lopore,''  as  indicating  a  distinct  disease  of  the  spinal  cord. 

The  cord  may  be  hoUov^^ed  out  very  quickly,  as  is  show^n 
by  the  folloviring  case  reported  by  Parkin : 

The  patient  was  standmg,  on  March  29th,  beneath  a  lift,  when 
the  chain  broke  and  the  lift  fell  on  his  head.  He  was  immediately 
rendered  unconscious,  and  remembers  no  more  about  the  accident. 
On  admission  to  the  hospital  there  were  no  signs  of  paralysis  of 
the  limbs,  but  in  eight  or  ten  hours  after  admission  the  left  arm 
was  found  to  be  weak,  and  rapidly  became  paralyzed.  On  March 
30th  there  was  anaesthesia  over  both  legs  and  arms,  said  to  be  only 
partial.  He  could  move  the  right  arm  a  little,  but  not  the  left. 
Could  not  pass  his  urine.  Catheter  had  to  be  used  twice  a  day. 
Motions  passed  involuntarily.  Temperature  subnormal.  April  2d  : 
Left  arm  completely  paralyzed.  Left  leg  stiff,  but  moves  a  little. 
No  knee-jerk  on  left  side.  Plantar  and  epigastric  reflexes  present. 
April  6th:  Left  hemiplegia  has  become  complete;  anaesthesia 
about  the  same.     April  nth:  Died  in  about  the  same  condition. 


SPINAL   COLUMN    UNINJURED.  jtq 

(The  gradual  extension  of  paralytic  symptoms  in  this  case  was 
very  similar  to  that  frequently  observed  in  hgemorrhage  of  the 
brain.) 

Post-mortem. — Spinal  column  intact.  No  extra-meningeal  hgem- 
orrhage. On  making  section  of  the  cord  at  a  point  two  inches 
and  a  half  below  the  apex  of  the  fourth  ventricle,  it  was  found  to 
be  hollowed  out,  having  about  half  an  inch  of  healthy  periphery. 
The  cavity  contained  soft,  grumous  material,  evidently  altered 
blood,  which  escaped  on  section.  The  cavity  occupied  about  three 
quarters  of  an  inch  of  the  length  of  the  cord. 

It  still  remains  to  be  proved  whether  these  acutely  occur- 
ring hsemorrhagic  cavities  can  cause  the  symptoms  of  syrin- 
gomyelia, which  is  a  disease  characterized  by  chronic  cavity 
formation  in  the  gray  matter.  In  cases  in  which  the  haemor- 
rhage is  associated  with  a  fracture  of  the  vertebras  there  is 
so  much  direct  injury  to  the  spinal  cord  in  addition  to  the 
haemorrhage,  that  the  symptoms  indicate  a  lesion  of  both  the 
white  and  the  gray  matter ;  and  even  without  bone  lesion, 
if  the  blood  is  poured  out  so  extensively  that  it  seriously 
compresses  the  white  matter,  the  clinical  manifestations 
will  be  those  of  a  transverse  lesion.  But  when  the  white 
matter  has  been  affected  but  little  or  not  at  all,  and  the 
haemorrhage  appears  in  the  gray  matter  alone,  it  seems 
probable  that  if  the  patient  recovers  from  the  effects  of  the 
acute  injury  he  may  present  symptoms  which  are  the  re- 
sults of  lesions  limited  chiefly  to  the  gray  matter.  These 
symptoms  will  be  found  in  the  parts  of  the  body  receiving 
their  nerve  supply  from  the  segments  affected,  and  con- 
sist in  localized  paralyses  of  motion,  with  loss  of  reflexes 
and  degenerative  electrical  reactions ;  atrophy  and  trophic 
changes  and  dissociated  anaesthesia,  of  which  the  most  com- 
mon variety  is  a  loss  of  sensibility  to  temperature  and  pain, 
while  the  sensations  of  touch  are  normally  transmitted  and 
perceived. 

The  symptoms  of  syringomyelia  are  usually  more 
marked  on  one  side  than  on  the  other,  and  there  occasion- 


8o  ORGANIC   EFFECTS   OF   INJURY. 

ally  is  seen  the  Brown-Sequard  type,  which  consists  in  pa- 
ralysis of  motion  on  one  side  of  the  body  and  of  sensation 
on  the  other  side. 

Although  no  autopsy  has  as  yet  proved  that  a  central 
hsemorrhage  of  the  spinal  cord  can  cause  symptoms  similar 
to  those  observed  in  syringomyelia,  there  are  several  clinical 
cases  recently  reported  which  speak  very  strongly  for  such 
a  possibility.     Of  these,  one  by  Minor  may  be  mentioned: 

A  man,  twenty  years  of  age,  previously  healthy,  fell  a  dis- 
tance of  seven  and  a  half  feet,  and  two  days  later  was  brought  to 
the  hospital.  Examination  showed  no  evidences  of  lesions  to  the 
skull,  brain,  or  vertebrae,  but  disclosed  symptoms  which  can  best 
be  explained  by  a  small  haemorrhage  situated  in  the  gray  matter  of 
the  left  side  of  the  spinal  cord,  and  extending  from  the  sixth  cer- 
vical to  the  first  thoracic  segment.  There  was  paralysis  of  the  left 
arm  and  leg  and  paresis  of  the  right  arm,  with  diminution  of  elec- 
trical excitability  in  both  upper  extremities.  The  tendon  reflexes 
were  absent  on  the  left  side,  but  were  only  diminished  on  the 
right.  Trophic  disturbances  were  present  about  the  shoulders. 
The  sensory  abnormities  were  the  most  interesting.  With  com- 
plete preservation  of  the  sense  of  touch  over  the  whole  body  and 
of  the  sense  of  pain  and  temperature  over  the  left  side,  there  was 
on  the  right  side  from  the  jaw  downward  a  profound  analgesia 
and  thermo-anaesthesia.  The  patient  recovered  almost  entirely 
from  the  paralysis  and  from  all  the  other  symptoms,  with  the  ex- 
ception of  the  loss  of  sensibility  to  pain,  which  remained  as  long 
as  the  case  was  under  observation.  (It  will  be  observed  that  the 
association  of  symptoms  in  this  case  is  very  similar  to  that  com- 
monly observed  in  syringomyelia.) 

In  some  cases  it  may  be  inferred  from  the  motor  symp- 
toms alone,  even  when  anaesthesia  is  totally  absent,  that  a 
small  hsemorrhage  has  occurred  and  has  remained  limited  to 
the  gray  matter. 

The  following  case,  a  patient  at  the  Vanderbilt  clinic 
whom  I  recently  presented  at  a  meeting  of  the  surgical  sec- 
tion of  the  New  York  Academy  of  Medicine,  illustrates  this  : 

The  patient,  who  is  seventeen  years  old,  was  a  strong,  healthy 
lad  until  the  summer  of  1895.     Then,  in  diving  from  a  dock  six 


SPINAL   COLUMN    UNINJURED.  8l 

feet  above  the  water,  he  went  too  straight  and,  the  water  being 
only  four  feet  deep,  struck  his  head  with  force  against  the  bottom. 
He  did  not  become  unconscious,  but  immediately  lost  power  in  all 
four  extremities.  He  was  pulled  out  of  the  water  by  other  boys, 
and  was  taken  home  and  put  to  bed.  For  three  days  he  lay  in 
bed,  unable  to  move  the  limbs  at  all,  with  pain  in  the  back  of  the 
neck  and  at  the  lower  part  of  the  spine.  There  was  retention  of 
urine  and  incontinence  of  faeces.  "  Pins  and  needles  "  in  the  left 
side  only.  No  loss  of  sensation.  No  involvement  of  the  face. 
After  three  days  the  right  side  began  to  improve  and  all  the  pain 
ceased.  In  four  months  the  patient  could  walk,  and  has  been 
gradually  improving  ever  since.  Now  (April  7,  1897)  there  are 
weakness  and  stiffness  in  the  intrinsic  muscles  of  the  hands  of  both 
sides,  very  much  more  marked  on  the  left.  The  left  hand  is  in 
the  pen  position  through  spasm  of  the  interossei,  and  the  interos- 
seous muscle  of  the  left  little  finger  is  paralyzed.  Electrical  reac- 
tions are  normal  except  for  the  extensors  of  the  fingers  and  for 
the  interossei  on  the  left  side;  m  these  muscles  electrical  ex- 
citability is  diminished.  There  is  a  slight  sinking  in  of  the  left 
interosseous  spaces.  The  other  muscles  of  the  arms  are  normal. 
The  right  leg  is  perfectly  normal,  but  the  left  leg  is  weak,  and  its 
muscles  are  in  a  condition  of  spastic  rigidity,  with  increased  reflexes 
and  ankle  clonus.  The  abdominal  and  plantar  reflexes  are  lost  on 
the  left  side.  As  the  patient  walks  the  left  leg  is  dragged  some- 
what and  circumducted  in  characteristic  hemiplegic  style.  There 
are  nowhere  any  changes  in  cutaneous  sensibility,  nor  tremor,  nor 
tenderness  of  the  back,  nor  external  evidences  of  any  injury  to 
the  spine. 

Thus  the  symptoms  which  remain  are:  Slight  flaccid  paralysis 
of  the  intrinsic  muscles  of  the  left  hand,  and  to  a  very  slight  de- 
gree of  the  muscles  of  the  right  hand;  spastic  paresis  of  the  left 
leg,  no  disturbances  of  cutaneous  sensibility,  no  evidences  of  in- 
jury to  the  spinal  column. 

Such  symptoms  permit  a  very  exact  localization  of  the  lesion. 
In  this  case  there  is  every  probability  that  there  was  a  slight 
haemorrhage  into  the  gray  matter  of  the  first  thoracic  segment  of 
the  spinal  cord,  chiefly  anteriorly  and  on  the  left  side.  An  oedema 
or  softening  quickly  developed,  so  that  for  a  time  the  patient  pre- 
sented the  symptoms  of  a  transverse  lesion.  These  soon  werit 
away,  however,  leaving  a  focal  lesion  which  involved  only  slightly 
the  anterior  horn  of  the  right  side,  but  destroyed  some  of  the  an- 
terior horn  on  the  left  side.     The  absence  of  sensory  symptoms 


g2  ORGANIC    EFFECTS   OF    INJURY. 

would  indicate  that  the  posterior  horn  and  the  central  canal  were 
not  involved.  The  haemorrhage  must  also,  either  directly  or  indi- 
rectly, have  impaired  the  conducting  power  of  the  left  pyramidal 
tract. 

In  the  cases  which  have  been  described  here,  and  in- 
deed, as  far  as  I  know,  in  all  hitherto  published  cases  of 
hsematomyelia,  the  hgemorrhage  has  been  focal.  Although 
the  blood  may  have  burrowed  for  long  distances  up  and 
down  the  gray  matter  of  the  cord,  the  columns  of  blood 
have  been  extensions  from  one  bleeding  point,  and  not  dis- 
tributed as  multiple  haemorrhages. 

Through  the  courtesy  of  Dr.  T.  J.  Larkin,  Assistant 
Pathologist  to  St.  Francis*  Hospital,  I  have  recently  had  the 
opportunity  of  examining  a  case  of  hsematomyelia  essen- 
tially different  from  any  previously  described.  In  this  case 
there  was  no  single  point  of  extensive  haemorrhage,  but 
the  spinal  cord  was  dotted  throughout  its  whole  extent  with 
microscopic  collections  of  free  red  blood  cells.  Although 
the  spine  was  fractured  at  one  point,  the  haemorrhages  were 
multiple  and  occurred  independently  of  the  bone  lesions,  so 
that  the  case  can  be  properly  described  in  this  section.  The 
facts  are  as  follows : 

A  workman,  after  receiving  a  severe  fall,  was  picked  up  un- 
conscious and  brought  to  the  hospital  in  deep  coma  and  paralyzed 
in  all  extremities.  He  died  in  three  hours  from  respiratory  fail- 
ure. At  the  autopsy  the  skull  was  found  intact,  but  there  was  a 
haemorrhage  in  the  middle  fossa.  There  was  a  fracture  disloca- 
tion of  the  atlas  and  axis  which  had  caused  extensive  mutilation 
of  the  second  and  third  cervical  segments  of  the  spinal  cord. 
There  was  no  haemorrhage  in  the  spinal  canal.  Except  at  the 
point  of  compression,  the  spinal  cord  looked  in  everyway  normal. 
The  membranes  were  not  lacerated,  the  contour  of  the  cord  was 
perfectly  preserved,  and  its  substance  was  firm  to  the  touch.  On 
section  it  could  be  seen  that  the  blood  vessels  were  somewhat 
prominent,  but  the  eye  could  detect  no  haemorrhage  either  at  the 
seat  of  injury  or  in  lower  levels.  All  the  other  organs  appeared 
perfectly  normal  and  free  from  haemorrhage.     Through  a  misun- 


SPINAL   COLUMN    UNINJURED.  8^ 

derstanding  on  the  part  of  the  dead-house  attendant,  the  upper 
portion  of  the  cord  was  thrown  away,  so  that  the  microscopic  ex- 
amination was  hmited  to  the  thoracic  region  and  regions  below  it. 
Sections  were  made  of  every  segment  of  the  thoracic,  lumbar,  and 
sacral  regions,  and  of  the  conus  terminalis,  which  had  been  hard- 
ened in  Miiller's  fluid  and  formalin,  and  which  were  then  exam- 
ined microscopically  by  means  of  the  picro-acid-fuchsin  method. 
The  lesions  found  were  generally  distributed  up  and  down  the 
cord,  and  consisted  of  recent  capillary  haemorrhages,  which  were 
so  minute  that  they  could  not  have  been  detected  by  the  naked 
eye.  No  single  hgemorrhage  contained  over  two  or  three  hundred 
blood  cells,  and  the  majority  of  them  contained  fewer.  In  some 
places  there  were  only  two  or  three  free  cells.  In  a  few  sections 
the  blood  lay  in  little  cavities,  but  the  most  common  distribution 
of  it  was  in  the  form  of  an  infiltration  of  a  small  number  of  blood 
cells  between  the  neuroglia  and  nerve  fibers.  There  was  nowhere 
any  tubular  cavity  formation.  The  largest  extravasations  were 
in  the  pia  and  around  the  nerve  roots.  In  the  spinal  cord,  al- 
though occurring  in  the  gray  matter,  they  were  most  frequent  in 
the  white  matter,  especially  in  the  posterior  columns.  Nearly  every 
section  contained  the  haemorrhages,  but  no  section  contained  very 
many,  usually  not  more  than  two  or  three.  The  situation  of  the 
haemorrhages  bore  little  or  no  relation  to  the  location  of  the  large 
blood-vessels.  The  blood-vessels  were  prominent  and  filled  with 
blood.     In  all  other  respects  the  spinal  cord  appeared  normal. 

Thus,  to  briefly  resume,  a  healthy  man  fell  with  sufficient  vio- 
lence to  break  his  neck  and  to  cause  an  intracranial  haemorrhage 
without  fracture  of  the  skull.  The  force  was  exerted  chiefly  on 
the  atlas  and  axis,  as  seen  by  the  injury  to  these  bones.  But  it 
was  also  adequate  to  cause  throughout  the  cord  punctate  haemor- 
rhages, which  were  entirely  unassociated  with  the  severe  local  in- 
jury and  which  were  probably  due  to  the  general  violence  to 
which  the  whole  spinal  cord  was  subjected.  That  injury  can 
cause  minute  and  multiple  lesions  in  the  spinal  cord,  without  frac- 
ture of  the  vertebrce,  has  often  been  assumed,  but,  as  far  as  I  know, 
never  before  been  demonstrated. 

The  proof  of  such  a  possibility  is  of  great  importance  for  the 
possible  explanation  of  the  pathology  of  the  obscure  cases  of  sus- 
pected spinal  disease  in  which,  after  severe  accidents,  the  patients 
give  symptoms  of  serious  impairment  of  spinal-cord  function  with- 
out definite  signs  of  circumscribed  injury.  In  the  present  case  the 
lesions  of  vital  centers  completely  masked  any  clinical  symptoms 


g^  ORGANIC  EFFECTS  OF  INJURY. 

which  the  capillary  haemorrhages  might  otherwise  have  caused. 
Had  the  violence  acted  so  that  there  had  been  no  gross  lesions,  it 
might  be  that  the  small  haemorrhages  would  have  given  rise  to 
symptoms  indicative  of  multiple  and  minute  foci  of  structural 
damage  to  the  spinal  cord. 

Concussion  or  Commotion  of  the  Spinal  Cord. 

As  a  designation  for  a  pathological  entity,  the  term  con- 
cussion or  commotion  of  the  spinal  cord  should  be  limited 
to  such  conditions  as  may  occur  as  a  result  of  injuries 
to  the  back,  or  of  general  concussion  accidents,  and  vv^hich 
have  not  been  caused  by  pressure  from  displaced  fragments 
of  the  spinal  column  or  by  hgemorrhage  in  the  spinal  canal 
or  into  the  substance  of  the  spinal  cord.  The  time  has 
gone  by  when  intelligent  physicians  were  deceived  by  the 
supposed  resemblance  between  such  general  functional  affec- 
tions as  hysteria  or  neurasthenia  and  concussion  of  the 
spinal  cord.  Concussion,  however,  continues  to  be  invoked 
as  an  explanation  for  certain  cases  of  organic  paraplegia 
which  are  probably  due  to  lesions  much  coarser  than  molec- 
ular disarrangement.  The  pathological  condition  with  which 
it  is  most  liable  to  be  confused  is  haemorrhage,  and  to  at- 
tempt to  distinguish  between  conditions  so  closely  allied 
may  at  first  seem  to  be  of  the  nature  of  a  pathological  quib- 
ble. Recent  acquisitions  to  our  knowledge  of  hsematomyelia 
have  shown,  however,  that  such  a  distinction  is  imperative 
if  we  are  to  get  at  the  truth  of  the  influence  of  trauma  in 
the  pathogenesis  of  the  obscurer  forms  of  spinal-cord  dis- 
eases. Hsemorrhage  usually  occurs  first  in  the  gray  mat- 
ter, and  generally  remains  localized  there.  If  fibers  are 
injured  without  haemorrhage,  as  the  believers  in  spinal  con- 
cussion maintain,  it  would  seem  reasonable  to  suppose  that 
the  resulting  symptoms  would  be  different  from  those  of 
hasmatomyelia. 

Does  such  a  condition  as  spinal  concussion  exist?     In 


CONCUSSION    OR    COMMOTION   OF    THE    SPINAL   CORD.      85 

Other  words,  can  any  violence  be  sufficiently  severe  to  cause 
direct  injury  exclusively  to  the  essential  elements  of  the 
spinal  cord?  To  this  question  a  positive  answer  is  yet  to  be 
given.  As  is  well  known,  lesions  of  all  grades  of  severity 
may  follow  compression  by  bony  splinters  or  by  blood  clots 
in  the  spinal  canal,  and  intraspinal  haemorrhage  may  occur 
without  there  being  any  discoverable  pathological  changes 
in  the  nerve  fibers,  other  than  those  explainable  by  the  effects 
of  pressure.  But  these  are  well-recognized  conditions,  and 
are  the  results  of  laceration  and  compression,  and  do  not  re- 
quire to  be  explained  by  the  assumption  of  concussion. 

The  question  is  not  whether  the  fibers  which  compose 
the  spinal  cord  are  of  different  function  and  amenable  to 
different  laws  than  are  nerve  fibers  situated  elsewhere,  but 
whether  they  ai-e  not  so  securely  protected  that  an  injury 
can  not  reach  them  without  having  first  fractured  or  dislo- 
cated bone  or  having  caused  rupture  of  blood-vessels. 

The  nerve  fibers  of  the  spinal  cord  of  course  differ  in  no 
essential  respects  from  those  of  the  brain  or  of  the  periph- 
eral nerves.  They  serve  purposes  of  conduction  and  obey 
general  physiological  laws;  yet  a  blow  on  the  head,  with- 
out causing  fracture  of  the  skull  or  visible  damage  to  the 
brain,  may  cause  symptoms  of  cerebral  concussion,  and  a 
blow  on  a  peripheral  nerve  is  frequently  followed  by  loss  of 
conductivity  in  it  without  there  being  any  gross  injury  to 
its  structure.  With  the  spinal  cord,  however,  the  case  is 
different.  The  back  often  receives  severe  injuries  without 
there  resulting  any  symptoms  referable  to  the  spinal  cord. 
The  explanation  of  the  fact  that  violence  applied  to  the 
back  rarely  if  ever  results  in  symptoms  of  spinal-cord 
lesions  which  can  not  be  explained  by  laceration  or  com- 
pression, is  to  be  sought  for  in  the  immunity  from  any  but 
the  severest  injuries  afforded  that  organ  by  the  protecting 
structures  which  surround  it. 

Accordingly,  while  we  are  not  in  a  position  to  unquali- 
7 


86  ORGANIC   EFFECTS   OF   INJURY. 

fiedly  assert  that  spinal  concussion  can  not  occur,  we  can  say 
that  if  it  occurs  at  all  it  is  certainly  one  of  the  rarest  of  acci- 
dents to  the  nervous  system — a  fact  which  is  amply  estab- 
lished by  experience,  and  which  may  be  explained  by  the 
anatomy  of  the  cord  itself  and  of  the  surrounding  parts.  In 
by  far  the  larger  number  of  cases  the  spine  is  fractured,  and 
the  only  cord  symptoms  are  those  referable  to  a  nervous 
lesion  in  the  immediate  vicinity  of  the  bone  lesion.  We 
never  hear  of  cases  of  compression  of  one  part  of  the  cord 
and  of  concussion  in  a  part  higher  up  ;  on  the  contrary^ 
spinal-cord  injuries  are  characterized  by  the  contrast  be- 
tween the  conditions  below  the  lesion  and  those  above  it. 

The  literature  of  spinal  concussion  is  voluminous,  but 
trustworthy  facts  are  few. 

In  the  cases  which  have  been  regarded  as  reliable  ex- 
amples of  the  condition  by  A.  Westphal,  and  by  Willard  and 
Spiller,  the  vertebrae  were  fractured,  and  there  were  cord 
lesions  with  haemorrhages  in  the  immediate  vicinity  of  the 
fracture.  These  investigators  maintained  that  the  cord 
lesion  was  the  result  of  "  concussion  "  and  not  of  compres- 
sion by  loosened  vertebrae.  They  based  their  opinions  upon 
the  absence  of  evidences  of  external  bruising  to  the  cord. 

If  such  proof  is  to  be  accepted  as  evidence  the  condition 
must  be  regarded  as  not  uncommon,  for  every  pathologist 
is  familiar  with  the  fact  that  the  spinal  cord  frequently 
retains  its  normal  contour  after  it  has  been  momentarily 
though  seriously  compressed.  That  slight  and  temporary 
compression  is  amply  sufficient  to  cause  a  loss  of  spinal  func- 
tion is  shown  by  the  frequency  with  which  complete  para- 
plegia results  from  spinal  operations  when  the  spinal  cord 
has  been  merely  touched  by  the  finger  of  the  operator.  To 
disregard  the  action  of  so  well-recognized  a  cause  as  frac- 
ture, as  is  done  by  the  above-mentioned  authors,  which  was 
in  their  cases  present,  and  to  assume  the  action  of  another 
and  unproved  cause,  appears  to  me  unjustifiable. 


CONCUSSION   OR   COMMOTION    OF    THE    SPINAL   CORD. 


87 


Gowers  is  the  warmest  partisan  of  the  theory  of  spinal 
concussion,  and  one  is  tempted  to  accept  as  final  the  opinion 
of  so  illustrious  a  neurologist.  Yet  the  proofs  which  he 
adduces  are  far  from  satisfactory.  Most  of  the  cases  he 
cites  date  from  a  period  whose  neurological  contributions 
must  be  accepted  with  considerable  reserve.  In  one  of 
the  more  recent  ones  (Fischer)  there  was  an  extra-dural 
haemorrhage,  extending  from  the  cervical  to  the  lumbar 
regions,  of  which  Gowers  makes  no  mention.  Gowers's 
own  case  is  so  interesting  that  it  is  to  be  regretted  that  it  is 
not  reported  a  little  more  in  detail. 

"  A  lady  was  severely  shaken  in  a  railway  collision.  She 
seemed  immediately  after  the  accident  to  have  suffered  no 
injury,  but  in  a  few  days  paraplegia  developed,  and  from 
its  consequences  she  died  six  weeks  after  the  accident. 
Throughout  the  dorsal  regions  of  the  cord  I  found  indica- 
tions of  subacute  myelitis  chiefly  in  the  white  columns, 
varying  in  its  extent  in  diffefent  regions,  but  in  most  part 
confined  to  the  lateral  tracts."  In  the  absence  of  fuller  de- 
tails, this  case  can  hardly  be  accepted  as  proof  of  spinal 
concussion  ;  the  softening  might  equally  well  have  been  the 
late  results  of  hcemorrhage. 

The  celebrated  researches  of  Schmaus  have  been  gener- 
ally received  as  finally  settling  the  question.  Schmaus  re- 
ports the  microscopic  examination  of  the  spinal  cords  of 
four  individuals  who  died  from  the  effects  of  traumatic  para- 
plegia. In  three  the  spinal  column  had  not  been  fractured. 
As  in  all  of  these  cases  the  patients  had  survived  the  injury 
and  had  lived  with  paralytic  symptoms  for  several  months,  in 
order  to  discover  the  early  stages  of  concussion,  Schmaus 
induced  paraplegia  in  animals  by  tapping  them  on  the  back 
with  a  hammer,  without  inflicting  injury  to  the  spinal  col- 
umn. As  the  result  of  his  investigations,  he  concluded  that 
"  anatomical  changes  of  the  specific  nerve  elements  may  be 
brought  about  by  purely  traumatic  means  ;  that  swelling  and 


88  ORGANIC  EFFECTS  OF  INJURY. 

degeneration  of  the  axis  cylinders,  breaking-  up  of  myelin, 
softening  and  gliosis,  with  cavity  formation,  may  result  di- 
rectly from  injury  independently  of  accessory  causes.  Hgem- 
orrhage  is  not  concerned  in  the  setiology,  but  may  appear 
as  an  accidental  or  secondary  accompaniment." 

Two  objections  must  be  overcome  before  Schmaus's 
conclusions  can  be  accepted,  as  proving  that  the  human 
spinal  cord  can  be  concussed.  One  of  them  is,  that  of  the 
human  cases  which  he  examined  all  presented  cavities  in 
the  gray  matter ;  and  inasmuch  as  they  did  not  come  to 
autopsy  till  a  long  time  after  the  injury,  the  probability  is 
very  strong  that  these  cavities  were  not  the  results  of  gliosis, 
as  Schmaus  interpreted  them,  but  were  spaces  which  were 
left  after  hsemorrhages  that  had  resulted  from  the  original 
injury  ;  and  that  the  cases  were  not  examples  of  concussion, 
but  were  forms  of  myelitis  secondary  to  hccmatomyelia. 

Schmaus's  animal  experimentation  seems  at  first  sight 
more  conclusive.  The  animals  became  paraplegic,  and  after 
death,  without  any  haemorrhages,  there  was  a  swelling  of 
the  axis  cylinders  in  the  parts  of  the  cord  opposite  the  seat 
of  external  injury. 

Experience  has  shown,  however,  that  the  utmost  con- 
servatism is  necessary  in  accepting  the  deductions  from 
experiments  upon  the  nervous  system  of  animals  as  appli- 
cable to  the  nervous  system  of  man.  In  guinea-pigs  and  in 
rabbits,  the  animals  that  Schmaus  made  use  of,  the  pro- 
tection of  the  spinal  cord  by  skin,  muscle,  bone,  and  liga- 
ments, after  due  allowance  is  made  for  comparative  differ- 
ences in  size,  is  very  much  less  secure  than  in  man.  And 
the  possibility  of  causing  paraplegia  without  gross  lesions 
in  these  animals  does  not  justify  the  conclusion  that  a 
similar  result  might  be  expected  were  man  the  animal  ex- 
perimented upon.  Schmaus's  results,  furthermore,  are  not 
identical  with  those  of  a  subsequent  observer,  Bikeles,  who, 
in  a  series  of   experiments  conducted   along  similar  lines, 


CONCUSSION    OR   COMMOTION   OF   THE   SPINAL   CORD.     89 

found  that  swelling  of  the  axis  cylinders,  a  condition  to 
which  Schmaus  attached  great  importance,  was  absent. 

Were  the  point  at  issue  one  as  to  whether  or  not  the 
fibers  and  cells  of  the  spinal  cord  were  susceptible  of  a  tem- 
porary depression  of  their  function  under  the  influence  of 
properly  applied  violence,  valuable  deductions  might  be 
drawn  from  animal  experimentation.  Such,  however,  as  has 
already  been  said,  is  not  the  question.  The  problem  has  to 
do  with  the  structures  which  protect  the  human  spinal  cord 
rather  than  with  the  functions  of  the  spinal  cord  itself,  and 
must  consequently  find  its  solution  in  the  hospital,  in  the 
dead  house,  and  in  the  laboratory  of  human  pathology. 

Leyden,  who  is  often  quoted  as  a  believer  in  concussion, 
now  regards  it  as  secondary  to  hsemorrhage. 

Such  is  the  most  important  evidence  for  the  existence 
of  the  pathological  condition  known  as  concussion  of  the 
spinal  cord.  The  writings  of  \yatson,  of  Vibert,  and  of 
many  others  who  are  frequently  cited  in  this  connection, 
can  not  be  regarded  as  having  materially  added  to  our 
knowledge  of  the  subject.  In  view  of  the  intense  interest 
with  which  the  question  has  been  for  so  many  years  sur- 
rounded, and  in  consideration  of  its  importance  both  to 
medicine  and  to  law,  the  facts  seem  very  meager. 

To  the  impartial  observer  the  conviction  must  be  inevi- 
table that  the  evidence  is  totally  insufficient  for  the  question 
to  be  accep)ted  as  proved,  although  the  weight  of  evidence 
is  against  the  existence  of  the  condition.  When  one  con- 
siders the  volumes  which  have  been  written  upon  the  sub- 
ject, the  medical  congresses  in  which  discussion  of  it  has 
held  the  prominent  place,  the  enormous  sums  of  money 
which  have  been  paid  for  it  in  damage  claims,  and  then 
turns  to  the  few  published  cases  which  are  advanced  as 
proof,  there  seems  to  be  a  great  disparity  between  the 
amount  that  is  known  about  it  and  the  amount  that  is  talked 
about  it. 


^O  ORGANIC  EFFECTS  OF  INJURY. 

If  traumatisms  ever  act  upon  the  spinal  cord,  so  that  its 
essential  elements  are  injured  without  being  compressed  by 
foreign  bodies  or  by  blood,  such  a  lesion  is,  from  the  pub- 
lished evidence,  among  the  rarest  of  nervous  pathology,  and 
by  no  means  entitled  to  the  position  of  promanence  it  has  so 
long  occupied. 

Symptoms  of  Spinal-cord  Injury. — The  symptoms  of 
acute  injury  to  the  spinal  cord  are  so  generally  familiar  that 
they  need  be  but  briefly  referred  to.  They  result  from  loss 
of  conductivity  and  from  disturbance  of  the  reflex  functions 
situated  in  that  organ.  There  are,  accordingly,  paralj^sis, 
almost  always  bilateral,  with  atrophy  and  degenerative  elec- 
trical reactions,  and,  as  a  later  result,  contractures.  At  first 
the  paralysis  in  the  affected  muscles  is  flaccid  and  usually 
complete.  When  the  limb  is  grasped  by  the  hand  of  the 
examiner  there  is  total  absence  of  all  resistance ;  if  lifted  up 
and  then  let  fall,  it  drops  like  a  dead  weight.  The  reflexes 
are  almost  always  lost  at  first.  Whether  they  remain 
absent,  or  return  and  become  exaggerated,  depends  upon 
the  altitude  and  extent  of  the  lesion,  ultimate  exaggera- 
tion of  the  tendon  reflexes  being  the  rule  in  lesions  above 
the  lumbar  enlargement.  Priapism  is  frequent.  The  faeces 
may  be  passed  involuntarily,  or  there  may  be  constipation. 
Similarly  there  is  retention  or  incontinence  of  urine.  Tro- 
phic and  vaso-motor  disturbances,  in  the  form  of  bedsores, 
cyanosis,  and  coldness  in  the  extremities,  are  prominent 
symptoms  in  most  cases. 

Pain,  either  at  the  seat  of  the  injury  or  radiating  down 
the  limbs,  is  in  my  experience  only  an  occasional  symptom. 
Anaesthesia  has  always  been  regarded  as  a  cardinal  symp- 
tom, but  it  is  through  the  studies  of  Starr,  Thorburn,  Sher- 
rington, Head,  and  still  more  recently  of  Kocher,  that  we 
have  learned  its  true  value.  It  has  been  conclusively  shown 
that  the  distribution  of  anaesthesia  due  to  spinal-cord  lesions 
is  entirely  different  from  that  caused  by  injury  to  the  brain 


SYMPTOMS   OF   SPINAL-CORD   INJURY. 


91 


or  to  the  peripheral  nerves,  or  from  that  observed  in  hys- 
teria. This  fact  is  of  paramount  importance  for  purposes 
of  diagnosis  between  affections  of  the  spinal  cord  and  con- 
ditions by  which  they  may  be  simulated,  as  w^ell  as  for  the 
localization  of  the  site  of  the  injury.      In  fractures  or  dis- 


FiG.  22.— Sensory  distribution  of  the  spinal-cord  segments  as  determined  by 
spinal-cord  lesions.     (After  Starr.) 

locations  of  the  spine  it  is  usually  impossible  to  determine 
from  such  external  evidences  as  mobility  or  deformities  of 
the  vertebras  the  exact  seat  of  the  lesion  in  the  spinal  cord. 
But  when  cutaneous  sensibility  is  lost,  as  it  almost  always  is 
in  these  cases,  the  topography  of  the  anaesthesia  may  be 
^confidently  relied  upon  to  furnish  a  means  for  the  determi- 


92 


ORGANIC   EFFECTS   OF   INJURY. 


nation  of  the  highest  spinal-cord  segment  which  has  lost  its 
power  of  transmitting  sensory  stimuli. 

The  sensory  supply  of  the  spinal-cord  segments  is  so 
constant  that  it  is  possible  to  construct  charts  that  indicate 


Fig.  23. — Sensory  distribution  of  spinal-cord  segments.     (After  Kocher. ) 

the  distribution  of  the  anaesthetic  areas  which  may  be  ex- 
pected in  ,  lesions  of  any  one  segment.  Although  the 
schemes  as  elaborated  by  different  observers  do  not  agree 
absolutely,  the  differences  are  unimportant  and  may  be  ex- 
plained by  the  fact  that  the  lesion  rarely  affects  a  segment 


SYMPTOMS   OF    SPINAL-CORD   INJURY. 


93 


exactly  according  to  its  anatomical  boundaries.  Figs.  22 
and  23  illustrate  the  areas  of  segmental  distribution  of  anaes- 
thesia as  laid  down  by  Starr  and  Kocher. 

A  transverse  lesion  of  one  segment  involves  a  loss  of 
conductivity  in  all  the  segments  below  it.  Thus  Fig.  24 
illustrates  the  areas  of  sensory  loss  in  a  case  of  fracture  of 
the  cervical  vertebras,  seen  by  me  in  consultation  with  Dr. 
P.  R.  Bolton.     There  was  a  transverse  lesion  at  the  eighth 


Fig.  24.— Anesthesia  in  a  case  of  fracture  of  the  cervical  vertebrae,  with  injury  to 
the  eighth  cervical  segment  of  the  spinal  cord.     (Hudson  Street  Hospital.) 


cervical  segment,  with  ansesthesia  in  the  distribution  of  that 
segment  and  in  all  segments  below  it.  Similarly,  in  a  patient 
of  my  own  who  is  still  living,  the  ancssthesia,  as  shown  in 
Fig.  25,  indicates  a  lesion  which  does  not  extend  above  the 
fifth  lumbar  segment.  The  characters  of  the  aucesthesia  after 
severe  injuries  are  constant.  With  the  exception  that  it  is 
less  at  the  upper  limits,  the  ansesthesia  is  usually  total  and 
complete,  so  that  sensations  of  touch,  pain,  or  temperature 
are  not  perceived  at  all,  and  that  the  sense  of  position  is  lost. 


94 


ORGANIC  EFFECTS  OF  INJURY. 


The  extent  and  distribution  of  the  various  clinical  mani- 
festations differ  with  the  extent  and  character  of  the  lesion. 
If  the  cord  has  been  seriously  bruised,  or  if  extensive  haemor- 
rhage has  occurred,  the  resulting  symptoms  appear  prompt- 
ly and  are  then  those  of  a  transverse  lesion.  If,  on  the  other 
hand,  the  damage  to  the  spinal  cord  has  been  slight  or  par- 
tial, the  symptoms  may  be  somewhat  delayed  in  appearing 
and  may  be  of  a  more  selective  character.     Anaesthesia  is 


Fig.  25. — Anaesthesia  in  a  case  of  a  fracture-dislocation  of  the  vertebrje,  with  injury 
to  the  fifth  lumbar  segment  of  the  spinal  cord.     (Incurable  Hospital.) 


always  present  in  severe  injuries,  but  when  the  other  symp- 
toms indicate  only  a  partial  lesion  anaesthesia  may  be  en- 
tirely absent. 

Thus,  in  a  case  seen  in  consultation  with  Dr.  G.  E.  Brewer,  the 
patient,  a  man,  forty-five  years  of  age,  had  fallen  downstairs, 
hitting  his  back,  and  being  generally  shaken  up.  The  left  radius 
was  fractured,  but  there  were  no  external  evidences  of  injury  to 
the  bones  of  the  spine.  The  patient  walked  about  for  two  hours 
after  the  accident,  but  then  "felt  his  legs  giving  out."  He  was 
obliged  on  this  account  to  stay  in  bed  at  first,  but  soon  partially 


SYMPTOMS   OF   SPINAL-CORD   INJURY.  q^ 

regained  the  use  of  his  limbs.  At  the  time  that  I  saw  him,  two 
weeks  after  the  accident,  he  could  walk  with  support;  the  knee- 
jerks  were  active,  especially  the  right ;  the  abdominal  reflexes  were 
absent;  there  was  a  large  bedsore  over  the  sacrum;  there  was  in- 
continence of  urine  and  faeces.  The  most  scrupulous  examina- 
tion of  cutaneous  sensibility  failed  to  reveal  any  abnormal  varia- 
tion of  that  function  for  either  touch,  heat,  cold,  pain,  or  the  sense 
of  position.  By  many  this  case  would  be  regarded  as  an  example 
of  concussion  of  the  spinal  cord  ;  but,  for  reasons  already  given, 
it  seems  to  me  more  correct  to  make  the  diagnosis  of  compression 
from  a  slight  dislocation  or  fracture,  or  from  haemorrhage. 

The  character  of  the  lesion  in  injuries  to  the  spinal  cord 
may  usually  be  correctly  inferred  if  there  are  evidences  of 
fracture  of  the  vertebras.  It  is  when  there  are  no  external 
indications  of  injury  to  the  spinal  column  that  it  becomes 
difficult  to  determine  in  what  way  the  function  of  the  spinal 
cord  has  become  impaired  or  lost.  We  are  then  unable  to 
distinguish  between  compression  by  bone,  or  hsemorrhage. 
We  onl}'  know  that  haemorrhage  is  particularly  frequent  in 
the  cervical  region,  and  that  a  gradual  extension  of  sj^mptoms 
may  be  due  to  blood  finding  its  way  up  or  down  the  cord. 

Bibliography. 

Bailey,  Three  Cases  of  Brown-Sequard  Paralysis.  New  York 
Med.  Jour.,  March  9,  1895. 

Ibid.,  Severe  Injuries  of  the  Spine.  New  York  Med.  Rec,  May, 
1897,  li,  p.  638. 

Bikeles,  Ref.  Schmidt's  Jahrb.,  1895,  248. 

Kocher,  Die  Lasionen  des  mensch.  Riickenmarks  bei  Verletz- 
ungen  der  Wirbelsaiile,  Mitt,  aiis  der  Grenzgeb.  der  M.  u.  C,  1896, 
i,  4. 

Lambret,  Un  cas  d'hematorachis  traumatique.  Bulletin  med.y 
1895,  p.  865. 

Levier,  Beit,  zur  Lehre  von  der  Riickenmarks  Apoplexie. 
Dissert.,  Bern,  1864. 

Leyden,  Klinik  der  Riickenmarks  Krank,  1875. 

Minor,  Klinische  Beobachtungen  iiber  centrale  Haematomyelie. 
Arch,  fiir  Psych.,  1896. 

Parkin,  Cases  of  Haematomyelia.  Guy's  Hosp.  Reports,  1891, 
xlvii. 


g5  ORGANIC   EFFECTS   OF   INJURY. 

Pfeiffer,  Ueber  Ruckenmarksblutungen  und  centrale  Haemato- 
myelie.  Zusammenfassendes  Referat,  Cblatt.  fiir  allg.  Path,  und 
path.  Anat.,  September  15,  1896. 

Schmaus,  Beitrage  zur  path.  Anat.  der  Riickenmarkserschut- 
terung.     Virchow's  Archiv,  cii,  1890,  p.  326. 

Sherrington,  Philosoph.  Trans.,  1893,  vol.  184. 

Starr,  A  Contribution  to  the  Subject  of  Tumors  of  the  Spinal 
Cord.     Am.  Jour.  Med  Sc,  June,  1895. 

Thorburn,  A  Contribution  to  the  Surgery  of  the  Spinal  Cord, 
London,  1889;  zdi'd.,  Brain,  1894. 

Van  Gieson,  La  Semaine  me'dicale,  1894;  N'e7v  York  Med.  Jour. ^ 
1894  ;  Report  of  New  York  Neurological  Society,  1894. 

Vibert,  Etude  medico-l^gale  sur  les  blessures,  Paris,  1888. 

Watson,  Experimental  Study  of  Diseases  arising  from  Severe 
Concussions. 

A.  Westphal,  Ueber  einen  Fall  von  traum.  Myelitis.  Arch,  fiir 
Psych.,  1896,  xxviii,  p.  554. 

Willard  and  Spiller,  Concussion  of  the  Spinal  Cord.  New 
York  Med.  Jour.,  March  6,  1897. 


CHAPTER    III. 

INJURIES   TO   THE   PERIPHERAL   NERVES. 

Degeneration  and  inflammation  of  the  peripheral  nerves 
may  result  from  a  variety  of  causes,  but  only  those  forms  of 
peripheral  nerve  disturbance  vi^hich  are  the  effects  of  direct 
and  immediate  violence  will  be  considered  here.  The  path- 
ological changes  that  occur  in  a  nerve  w^hich  has  been  di- 
vided, and  so  cut  off  from  its  trophic  center,  can  not  be 
detected  w^ith  the  microscope  before  the  expiration  of  five 
to  eight  days.  Then  the  myelin  surrounding  the  axis  cylin- 
der may  be  seen  to  be  breaking  up,  a  process  of  degeneration 
which  progresses,  and  which  may  be  ultimately  associated 
with  the  destruction  of  the  axis  cylinder  and  replacement  of 
nervous  tissue  by  connective  tissue.  Such  a  process,  which 
may  occur  in  varying  degrees  as  the  result  of  crushes,  cuts, 
blows,  or  strains,  is  degenerative  rather  than  inflammator}^ 
and  it  is  only  by  the  addition  of  infectious  elements  (as  may 
occur  in  extensive  crushes  without  external  wound,  or  when 
there  is  a  wound  of  the  skin  as  well  as  injury  to  the  nerve) 
that  to  the  degeneration  of  nerve  fibers  are  added  the  ordi- 
nary vascular  manifestations  of  inflammation.  Nerve  disor- 
ders which  take  place  under  these  latter  conditions  may 
properly  be  called  traumatic  neurites,  but  the  simple  degen- 
erative process  should  be  spoken  of  as  nerve  degeneration, 
or  palsy,  and  not  as  nerve  inflammation. 

When  nerves  are  cut,  regeneration  may  occur  if  the  ends 
are  properly  united.  Repair  in  nerves  injured  by  blows  or 
crushes,  but  not  divided,  may  ordinarily  occur  in  the  course 

97 


p8  ORGANIC   EFFECTS   OF   INJURY. 

of  several  months.  In  both  these  cases  there  may  be  resto- 
ration of  function  in  varying  degrees. 

Loss  of  conducting  power  is  the  most  important  symp- 
tom of  degeneration  of  nerves.  The  anterior  and  posterior 
roots  of  the  spinal  nerves  conduct  impulses  of  different 
kinds,  but  the  union  of  the  motor  and  sensory  roots  occurs 
so  soon  after  their  exit  from  the  spinal  cord  that  most  pe- 
ripheral nerves  and  all  spinal  nerves  are  mixed  nerves,  and 
consequently  peripheral  nerve  palsies  almost  always  present 
symptoms  of  disorder  of  both  sensory  and  motor  function. 
The  trophic  centers  for  the  posterior  roots  are  in  the  spinal 
ganglia,  and  so  extra-medullary  ;  those  for  the  anterior  roots 
are  in  the  anterior  horns  of  the  spinal  cord.  Thus  there  are 
different  degenerating  paths  for  the  two  sets  of  root  fibers. 
But  these  are  differences  which  do  not  appear  in  the  clinical 
picture,  because  simple  traumatic  lesions  affect  the  nerves 
outside  the  spinal  canal,  and  consequently  external  to  the 
trophic  centers  for  both  sensory  and  motor  nerves. 

^Etiology. — Nerves  may  be  injured  by  being  cut,  lacer- 
ated, bruised,  stretched,  or  compressed.  The  most  frequent 
injuries  are  bullet  wounds,  cuts  from  sharp  instruments  or 
pieces  of  glass,  falls,  excessive  muscular  action,  and  pressure 
from  various  causes. 

In  the  severer  forms  of  traumatisms  the  general  condi- 
tion of  the  patient  has,  of  course,  but  little  influence  upon 
the  development  of  paralytic  symptoms.  But  slight  blows, 
falls,  and  pressure  effects  are  very  much  more  likely  to  be 
followed  by  loss  of  peripheral  nervous  function  in  enfeebled 
and  alcoholic  persons  than  in  persons  in  robust  health.  In 
pressure  palsies,  particularly,  alcohol  is  a  potent  predispos- 
ing agent. 

Symptoms. — Disturbances  of  motion  are  the  most  impor- 
tant symptoms  of  peripheral  nerve  injuries,  and  they  are 
such  as  are  caused  by  interference  with  the  lower  motor 
neuron.     Loss  of  conductivity  in  the  neuraxon  abolishes  the 


INJURIES   TO   THE    PERIPHERAL   NERVES. 


99 


transmission  by  it  of  the  impulses  of  motion  and  nutrition, 
so  that  the  muscles  are  paralyzed  and  undergo  atrophy, 
although  the  cell-body  portion  of  the  neuron,  situated  in  the 
spinal  cord,  remains  unaffected.  Although  the  motor  symp- 
toms of  peripheral  nerve  palsy  are  in  many  ways  similar  to 
those  which  may  result  from  disease  of  the  spinal  cord  itself, 
they  differ  so  essentially  in  distribution  and  in  association 
with  other  symptoms,  that  there  is  rarely  any  difficulty  in 
determining  whether  it  is  the  spinal  or  peripheral  part  of 
the  neuron  which  is  involved  by  the  lesion. 

Although  in  all  injuries  to  the  spinal  nerves  there  is 
usually  an  association  of  both  sensory  and  motor  symptoms, 
motor  paralysis  is  the  most  pronounced  and  the  most  impor- 
tant. It  occurs  immediately  or  soon  after  the  injury,  and  is 
always  flaccid  in  character.  It  is  limited  to  the  muscles  sup- 
plied by  the  injured  nerve,  although  usuallv  all  the  muscles 
are  not  involved  to  an  equal  degree.  Complete  loss  of 
power  of  a  whole  limb  is  only  observed  in  cases  in  which  the 
injury  has  been  extremely  extensive  and  severe.  Muscular 
weakness  becomes  apparent,  not  only  through  the  inability 
to  perform  certain  movements,  but  through  various  abnor- 
mal positions  of  parts  deprived  of  their  muscular  power. 
Through  continuous  overaction  of  opposing  muscles  the 
paralyzed  muscles  may  eventually  become  tense  and  the 
tendons  of  the  overacting  muscles  prominent,  thus  forming 
contractures  ;  but  spasticity,  such  as  is  ordinarily  seen  in 
cerebral  palsies,  never  occurs.  Deformities  may  result  from 
the  overaction  of  the  opposing  muscles,  as  is  seen  by  the 
drawing  of  the  mouth  to  one  side  in  facial  paralysis,  or  from 
the  effects  of  gravity,  as  is  the  case  with  the  drop-wrist  of 
"  Saturday-night  "  paralysis. 

Atrophy  in  muscles  slightly  paralyzed  often  does  not  ap- 
pear at  all,  but  when  a  nerve  has  been  seriously  injured  its 
occurrence  is  constant.  A  gentleman  was  alarmed  con- 
cerning atrophy  of  the  interossei  of  one  hand  and  beginning 


100  ORGANIC  EFFECTS  OF  INJURY. 

main  en  griff e ;  the  atrophy  was  very  marked,  and  had  all 
the  appearance  of  a  progressive  muscular  atrophy,  but  the 
condition  was  one  of  pressure  palsy  of  the  ulnar  nerve, 
due  to  injury  received  while  the  patient  was  under  ether 
for  an  operation  for  appendicitis  a  month  previously. 
After  injury  to  a  peripheral  nerve  the  muscles  may  occa- 
sionally very  soon  lose  their  firmness  and  consistency  ;  it  is 
usually,  however,  two  or  three  weeks  before  the  atrophy 
becomes  apparent  to  the  eye. 

Tremor  is  a  frequent  symptom  of  peripheral  nerve  in- 
jury ;  it  occurs  in  the  smaller  muscles  of  the  hand,  but  more 
frequently  after  traumatisms  affecting  the  muscles  around 
the  shoulder  joint.  It  is  fine,  fibrillary,  and  very  much  in- 
tensified by  movement  and  fatigue. 

Sensory  symptoms  are  not  usually  prominent  in  trau- 
matic palsies  of  nerves ;  even  when  a  nerve  is  divided  anaes- 
thesia does  not  invariably  result.  In  very  few  of  the  isolated 
peripheral  palsies  which  have  come  to  my  notice  have  there 
been  any  sensory  symptoms  other  than  tingling  and  numb- 
ness in  the  areas  supplied  by  the  injured  nerves.  Percep- 
tion and  localization  of  touch,  pain,  and  temperature  are 
usually  little  or  not  at  all  impaired.  Anaesthesia  may  occur 
in  the  regions  supplied  by  the  nerve,  but  it  is  chiefly  found 
in  cases  in  which  inflammation  is  added  to  the  degenerative 
process,  or  in  which  the  nerve  injury  has  been  particularly 
severe.  The  same  is  true  of  spontaneous  pain.  Neuritis  can 
cause  most  intense  pain.  But  in  the  non-septic  palsies  of 
traumatic  origin  pain  is  only  an  occasional  symptom.  It  is 
sometimes,  however,  the  most  prominent  result,  so  that  the 
condition  is  spoken  of  as  traumatic  neuralgia  rather  than 
palsy.  This  is  particularly  frequent  after  injuries  to  the  fifth 
and  to  the  sciatic  nerves.  Tenderness  over  the  affected 
nerve  trunk  and  muscles  is  also  occasionally  present,  and 
may  be  a  distressing  symptom.  In  lesions  of  the  sensory 
portions  of  nerves  it  is  the  lower  sensory  neuron,  which  is 


INJURIES   TO   THE    PERIPHERAL   NERVES.  loi 

•situated  between  the  posterior  spinal  ganglion  and  the  pe- 
riphery, that  is  affected.  Consequently,  when  it  is  injured, 
the  symptoms  of  disturbed  function  occur  in  the  course  of 
the  nerves  themselves.  From  the  description  of  anaesthesia 
and  paraesthesia  resulting  from  spinal-cord  injury,  it  will 
thus  be  seen  that  the  distribution  of  sensory  symptoms  is 
entirely  different  in  lesions  of  the  peripheral  nerves  from 
that  observed  in  lesions  of  the  spinal  cord. 

The  tendon  reflexes  in  peripheral  nerve  palsies  usually 
remain  unchanged,  because  the  muscles  concerned  in  reflex 
action  are  rarely  involved  in  these  disorders.  There  is 
never  any  increase  of  reflex  activity,  although  a  degenerat- 
ing muscle  may  contract  to  slight  mechanical  stimuli.  The 
knee-jerk  is  the  only  tendon  reflex  constantly  present  in 
health,  and  an  isolated  peripheral  palsy  of  the  extensors  of 
the  leg  is  extremely  rare. 

Electricity  is  the  most  valuable  agent  at  our  disposal  for 
the  diagnosis  and  prognosis  of  peripheral  nerve  injuries.  It 
is  only  in  disease  or  injury  of  the  lower  motor  neuron  that 
the  reaction  of  degeneration  occurs ;  in  primary  disease  of 
the  muscles  and  in  cerebral  palsies  electrical  irritability 
remains  practicalh'  unchanged.  All  severe  injuries  of  the 
peripheral  nerves,  however,  like  those  of  the  spinal  cord, 
are  associated  with  changes  in  electrical  reactions.  When 
the  protoplasmic  portions  of  the  neuron  (the  anterior  horn 
cells)  are  extensively  destroyed,  as  in  infantile  spinal  pa- 
ralysis, degenerative  reactions  are  constant  and  occur  rap- 
idly, but  in  chronic  affections  of  the  anterior  horns — e.  g., 
progressive  muscular  atrophy — the  cells  degenerate  slowly 
and  individually,  and  consequently  electrical  excitability  of 
the  muscles  is  retained  for  a  long  time,  and  only  disappear 
when  all  the  muscle  fibers  have  atrophied. 

The  electrical  examination  of  every  case  of  peripheral 
nerve  palsy  is  indispensable  for  clinical  purposes,  and  should 
be  carried  out  with  both  the  faradic  and  galvanic  current. 


I02  ORGANIC   EFFECTS   OF    INJURY. 

The  changes  in  electrical  excitability  after  injuries  to  the 
peripheral  neuron  have  already  been  described  (page  42). 
They  vary  in  character,  time  of  appearance,  and  duration, 
but  the  variations  are  usually  in  direct  ratio  to  the  extent  of 
injury.  After  severe  injuries  the  initial  period  of  hyper- 
excitability  is  short ;  after  slight  injuries  it  may  continue  for 
several  weeks  and  then  return  and  remain  at  the  normal. 
If  after  six  to  eight  days  there  is  no  decrease  of  excitability, 
we  may  infer  that  recovery  will  be  complete  and  rapid.  If 
after  two  weeks  the  faradic  irritability  of  the  nerve  is  en- 
tirely lost,  the  duration  of  the  paralysis  will  be  long.  In 
severe  injuries  there  may  be  for  several  months  no  response 
to  faradism  or  to  galvanism  applied  to  the  nerve,  or  to  fara- 
dism  applied  to  the  muscle,  while  the  galvanic  reactions  in 
the  muscles  may  be  increased  or  reversed.  If  after  three 
or  four  months  these  electrical  alterations  persist,  and  if  at 
the  same  time  there  has  been  no  improvement  in  the  paraly- 
sis, it  is  always  certain  that  recovery,  if  it  occurs  at  all,  will 
not  be  complete.  Very  frequently,  however,  there  is  a  re- 
turn of  motor  power  before  there  is  any  improvement  in 
the  degenerative  reaction.  Such  a  return  renders  the  prog- 
nosis more  favorable. 

Vaso-motor  and  trophic  disturbances  are  common  accom- 
paniments of  severe  injuries  to  nerves,  and  consist  in  the 
condition  known  as  glossy  skin,  in  oedema,  in  the  impair- 
ment of  the  growth  of  the  nails,  in  the  lowered  vitality  of 
the  skin  as  shown  by  the  occurrence  of  cutaneous  inflamma- 
tion and  subnormal  temperature,  and  by  the  atroph}^  of 
muscle. 

Prognosis.— The  prognosis  of  nerve  injury  depends  upon 
the  general  health  of  the  patient  and  the  extent  of  injury  to 
surrounding  parts  and  to  the  nerve  itself. 

Regeneration  of  nerves  occurs  more  quickly  in  the  robust 
than  in  the  person  exhausted  from  any  cause.  Injury  to  sur- 
rounding parts  interferes  with  the  reparative  process. 


INJURIES    TO    THE    PERIPHERAL   NERVES.  103 

The  extent  and  character  of  injury  which  the  nerve 
itself  receives  are  naturally  the  most  important  prognos- 
tic considerations.  From  the  effects  of  gradual  pressure, 
as  in  the  "  sleep  palsies,"  the  nerve  usually  recovers  per- 
fectly in  a  few  weeks  or  months.  From  the  effects  of 
severe  lacerations  the  return  to  normal  function  is  slower 
and  more  imperfect.  Even  from  complete  nerve  section 
fairly  good  recovery  is  possible,  if  the  ends  become  ap- 
proximated, although  it  is  always  tedious. 

It  is  impossible  to  give  a  certain  prognosis  in  severe  in- 
juries to  nerves  until  sufficient  time  has  elapsed  to  permit 
us  to  be  guided  by  electrical  reactions. 

The  importance  of  paralysis  of  the  cranial  nerves,  for 
purposes  of  cerebral  localization,  has  already  been  men- 
tioned. Some  of  them  are,  although  infrequently,  involved 
by  injuries  of  the  head  and  neck.  Any  of  the  superficial 
branches  of  the  fifth  nerve  may  be  paralyzed  by  blows  or 
cuts  on  the  face.  The  pneumogastric  has  been  injured, 
without  life  being  lost,  by  stabs  and  bullets.  Paralysis  of 
the  spinal  accessory,  with  consequent  loss  of  power  in  the 
sterno-cleido-mastoid  or  trapezius  muscles,  or  in  both  mus- 
cles, is  an  occasional  result  of  stabs  in  the  neck.  Lesions 
of  this  nerve  may  be  associated  with  lesions  of  the  hypo- 
glossal or  pneumogastric.  The  facial  and  hypoglossal  are 
the  most  important  of  the  cranial  nerves  frequently  injured, 
and  consequently  they  are  the  only  cranial  nerve  palsies 
which  will  be  described  in  detail. 

Facial  Nerve. — Traumatic  peripheral  facial  paralysis  is 
not  very  common.  Blows  on  the  ear  or  over  the  mastoid 
process,  stabs  or  cuts  in  this  region,  or  fractures  of  the 
jaw,  may  cause  paralysis  in  all  the  peripheral  branches  of 
the  nerve.  Injury  to  the  face  may  cause  loss  of  power  in 
either  of  the  facial  branches.  A  lady  was  operated  upon 
by  infraorbital  incision  for  i-ebellious  one-sided  neuralgia  of 


I04  ORGANIC   EFFECTS  OF    INJURY. 

the  fifth  nerve.  When  seen,  several  months  afterward,  the 
neuralgia  remained,  but  to  it  had  been  added  an  incurable 
paralysis  of  the  same  side  of  the  lips  and  cheek ;  the  cervico- 
facial branch  of  the  seventh  nerve  had  been  cut  at  the 
operation. 

The  synnptoms  of  facial  palsy  vary  with  the  extent  of  in- 
jury. A  blow  on  the  ear  or  mastoid  ma}-  cause  paralysis 
of  all  branches.  Then  the  paralyzed  side  of  the  face  will 
be  flattened,  the  prominence  of  its  cutaneous  and  muscular 
folds  diminished,  and  the  face  drawn  toward  the  sound  side. 
The  eye  can  not  be  closed  because  of  loss  of  power  in  the 
orbicularis  palpebrarum,  a  condition  which  not  uncom- 
monly results  in  a  troublesome  conjunctivitis  and  exposes 
the  eye  to  injury  from  foreign  bodies.  The  forehead  can 
not  be  wrinkled  on  the  affected  side.  The  mouth,  when 
closed,  is  usually  drawn  toward  the  sound  side,  causing  an 
inequality  which  becomes  still  more  evident  when  the 
patient  laughs  or  opens  the  mouth  wide.  In  paralysis  of 
the  Tips  and  cheeks  the  patient  complains  that  food  runs 
out  of  the  paralyzed  side.  He  can  not  close  the  lips  per- 
fectly, as  may  be  shown  by  attempts  at  whistling,  etc.  If 
the  temporo-facial  branch  alone  is  affected,  the  paralysis 
will  be  limited  to  the  forehead  and  eye;  if  the  cervico- 
facial, to  the  lips,  cheek,  and  platysma  myoides.  Abnormal 
electrical  reactions  occur  very  quickl3^ 

Blows  around  the  ear  affecting  the  facial  nerve  may  also 
cause  deafness,  tinnitus  aurium,  and  dizziness,  indicating 
disturbances  of  the  auditory  nerve  ;  but  extracranial  facial 
paralysis  is  not  associated  with  symptoms  of  injury  to  any 
other  nerve  except  the  eighth.  The  taste  is  not  affected ; 
impairment  of  sensation  may  occur  in  the  posterior  auricu- 
lar region,  but  never  on  the  face. 

The  diagnosis  is  simple ;  cerebral  facial  palsy  never  in- 
volves the  occipito-frontalis  to  a  marked  degree  and  does 
not  seriously    interfere    with  the  muscular   movements   in- 


INJURIES   TO   THE    PERIPHERAL   NERVES.  105 

volved  in  the  display  of  the  emotions.  When  a  person  with 
cerebral  facial  palsy  laughs,  the  innervation  of  both  sides  of 
the  face  is  usually  almost  equal,  so  that  the  differences  of  the 
facial  folds  are  scarcely  perceptible  ;  also,  paralysis  of  the 
seventh  nerve,  when  of  cerebral  origin,  is  usually  associated 
with  hemiplegia  of  the  same  side.  In  nuclear  disease,  or  in 
injury  of  the  nerve  in  its  course  from  the  pons  to  the  exit 
from  the  skull,  there  are  usually  associated  symptoms  of 
palsy  of  other  cranial  nerves,  as  well  as  disturbances  of  taste 
or  salivary  secretion. 

Hysterical  facial  paralysis  is  very  rare,  and  is  always 
associated  with  other  hysterical  stigmata. 

The  prognosis  varies  with  the  character  and  extent  of 
the  injury.  If  the  nerve  has  been  cut,  it  will  not  regenerate 
unless  the  ends  become  approximated  soon  after  the  injury. 
Many  cases  do  not  entirely  recover  even  after  a  slight  blow. 
Gowers  reports  the  case  of  a  boy,  who  was  struck  behind 
the  ear  with  a  book,  in  whom  the  resulting  facial  palsy  was 
permanent.  The  prognosis  should  be  very  guarded,  and 
controlled  by  electrical  examination.  Cases  which  show  no 
sign  of  improvement  after  four  months  will  probably  never 
recover  entirely. 

Hypoglossal  Nerve. — Extracranial  traumatic  paralysis  of 
this  nerve  is  usually  unilateral  and  always  due  to  punctured 
or  pistol-shot  wounds.  That  traumatic  paralysis  of  the  h3'po- 
glossal  is  rarely  observed  may  be  accounted  for  by  the 
close  anatomical  relations  of  this  nerve  with  the  pneumo- 
gastric,  the  internal  jugular  vein,  and  the  internal  and  ex- 
ternal carotid  arteries.  Because  of  this  association,  most 
injuries  of  the  nerve  in  its  deep  course  prove  fatal  from  in- 
volvement of  one  or  other  of  those  important  structures. 
It  is  only  after  it  has  passed  under  the  occipital  artery,  to 
proceed  beneath  the  stylo-hyoid  to  the  tongue,  that  it  may 
be  injured  without  great  danger  of  involving  the  large 
blood-vessels  and  the  pneumogastric. 


Io6  ORGANIC  EFFECTS  OF  INJURY. 

A  patient  at  the  Vanderbilt  clinic  presented  classical  symp- 
toms of  left-sided  paralysis  of  the  tongue.  He  had  been  stabbed 
in  the  neck  several  years  before,  and  sought  medical  advice  for 
an  aneurism  of  the  left  occipital  artery.  The  stab  wound  must 
have  divided  the  nerve,  near  the  occipital  artery,  but  only  have 
caused  slight  injury  to  the  blood-vessel. 

Unilateral  hypoglossal  paralysis  abolishes  motor  power 
in  the  corresponding  side  of  the  tongue.  When  the  tongue 
is  protruded  it  deviates  toward  the  paralyzed  side.  Eating 
and  talking  may  thus  be  seriously  interfered  with.  Sensory 
and  gustatory  abnormities  do  not  occur.  The  affected  side 
of  the  tongue  diminishes  in  volume,  and  its  surface  is 
traversed  by  deep  furrows  in  which  collect  epithelium  and 
dried  secretions. 

Traumatic  hypoglossal  paralysis  can  only  be  cured  by 
operation. 

Cervical  Plexus. — Paralysis  of  the  diaphragm,  resulting 
from  injury  to  the  phrenic  nerve,  which  arises  from  the 
third,  fourth  and  fifth  cervical  nerve  roots,  is  the  one  im- 
portant symptom  of  injury  to  the  cervical  plexus.  The 
other  branches  of  the  cervical  plexus  are  chiefly  sensory  ; 
their  distribution  may  be  seen  by  reference  to  the  chart  (see 
Fig.  26).  Unilateral  paralysis  of  the  diaphragm,  although 
an  unusual  accident,  may  result  from  shot  wounds  and  stabs 
of  the  neck.  The  symptoms  are  dyspnoea  on  exertion  and 
unilateral  loss  of  the  abdominal  type  of  breathing.  Litten 
was  the  first  to  describe  a  bilateral  wavelike  movement 
caused  by  contraction  of  the  diaphragm,  which  may  be  seen 
on  the  thorax  of  normal  individuals.  The  movement,  which 
is  very  slight,  descends  from  the  sixth  rib  on  inspiration,  to 
occur  again  on  expiration.  It  is  n6t  visible  in  paralysis  of 
the  muscle.     The  prognosis  of  this  condition  is  grave. 

Posterior  Thoracic. — This  nerve  supplies  the  serratus 
magnus.  Although  isolated  paralysis  of  the  posterior  tho- 
racic is  not  common,  it  may  result  from  falls  on  the  shoul- 


N.  trig. 

Plexus  cervic. 
N.  S7ij>racla-uic. 


N.  Lumbo-ingr, 
|SJ.  Ilio-ingr. 


N.  cut.  lat. 
N.  "'5^. 


N.   cjii.^nst. 


R.   ctit.  lat. 
N.  peron. 

N.  saph. 1- 


N.  suralis. 
N.  plant,  lat. 
N.  plant,  mcd.  

nerves  for  cutaneous  sensibility 


N.  occip.  7naj.       \ 
N.   occip.  7nin. 
N.  Attric.->nagn. 

NN.  supraclainc.l 

R.  Dors.     N.   J/z«. 
N.   ax///. 


N.   ck/.  jnedialis. 
NN.   intercost. 

N.  ?-a.^. 

N.  i^^^-  medius. 

IM.   771USC.  cut. 
NN.  cm/,  cluniuin. 

N.  per/,  lig.sacro-tub. 

N.  ''«^. 

|S|.   vtedian. 


INJURIES    TO    THE    PERIPHERAL   NERVES.     '  107 

der  or  from  injuries  to  the  neck.  A  woman  at  the  Vander- 
bilt  clinic  developed  it  immediately  after  delivery.  Such 
occurrences  are  explained  by  compression  of  the  nerve 
through  muscular  contraction.  Traumatic  paralysis  of  the 
scrratus  magnus  is  always  unilateral.  The  symptoms  are 
characteristic.  At  rest  the  internal  edge  of  the  scapula  is 
prominent,  and  its  lower  angle  is  nearer  the  vertebrge  than 
on  the  unparalyzed  side.  When  the  arm  is  held  forward 
the  scapula  has  the  peculiar  prominent  position  which  has 
received  the  name  of  "  winged  scapula."  The  arm  can 
only  with  difficulty  be  raised  above  the  shoulder. 
Recovery  is  always  tedious  and  may  not  occur. 
Circumflex. — The  circumflex  nerve  supplies  the  deltoid 
and  is  sometimes  paralyzed  from  injuries  around  the  shoul- 
der. As  a  result  the  shoulder  is  flattened,  and  as  move- 
ments of  the  deltoid  become  impossible,  the  arm  can  hardly 
be  raised  at  all.  If  there  is  much  atrophy,  a  subglenoid  dis- 
location of  the  humerus  is  usually  present.  The  circumflex 
also  suppHes  the  teres  minor,  but  paralysis  of  this  muscle  is 
unimportant.  The  electrical  reactions,  sensory  symptoms, 
and  prognosis  in  paralysis  of  the  circumflex  are  similar  to 
those  of  other  nerves. 

Musculo-cutaneous  Nerve.— Isolated  paralysis  is  very 
rare.  The  motor  symptoms  are  referable  to  the  biceps  and 
the  brachialis  anticus,  and  the  sensory  symptoms  to  the 
sensory  distribution  of  the  nerve. 

Median  Nerve. — Isolated  paralysis  of  this  nerve  is  un- 
common, but  median-nerve  palsy  is  not  infrequently  associ- 
ated with  palsies  of  other  nerves  affected  by  injuries  around 
the  shoulder  joint. 

The  symptoms  are  paralysis  or  weakness  in  the  muscles 
supplied  by  the  nerve.  From  paralysis  of  the  pronators,  the 
arm  is  slightly  rotated  outward,  and  pronation  is  impaired 
or  impossible.  From  paralysis  of  the  flexor  carpi  radialis, 
flexor  sublimis  digitorum,  and   of  one  half  of  the  flexor  pro- 


I08  ORGANIC    EFFECTS   OF    INJURY. 

fundus  digitorum,  flexion  of  the  wrist  and  fingers  is  inter- 
fered with.  The  nerve  supply  by  the  ulnar  of  the  flexor  carpi 
ulnaris,  of  the  inner  half  of  the  flexor  profundus  digitorum, 
and  of  all  the  interossei,  permits,  when  the  ulnar  nerve  re- 
mains intact,  some  flexion  of  the  wrist  and  of  the  terminal 
phalanges  of  the  two  inner  fingers  and  flexion  of  the  first 
phalanges  of  all  the  fingers.  Through  overaction  of  the 
extensors  of  the  thumb  (posterior  interosseus)  and  of  the 
adductor  (ulnar)  the  thumb  assumes  the  position  of  exten- 
sion and  adduction,  being  in  the  same  plane  as  the  fin- 
gers. Sensory  symptoms  are  usually  unimportant ;  they 
occur  in  the  sensory  distribution  of  the  nerve.  According 
to  Bernhardt,  paralysis  of  this  nerve  is  frequently  associated 
with  trophic  disturbances  (atrophy,  glossy  skin,  etc.).  The 
electrical  reactions  and  prognosis  have  no  individual  charac- 
teristics. 

Ulnar  Nerve. — The  ulnar  nerve  arises  from  the  inner 
cord  of  the  brachial  plexus,  derived  from  the  eighth  cervical 
and  first  dorsal  segments  of  the  spinal  cord.  From  its  origin 
in  the  axilla,  until  it  passes  through  the  olecranon  groove, 
its  course  is  superficial.  In  the  upper  part  of  the  forearm 
it  is  covered  by  the  flexor  carpi  ulnaris,  but  in  the  lower 
half  of  the  forearm  it  is  covered  only  by  integument  and 
fascia.  Its  superficial  situation  renders  it  ver}^  liable  to  in- 
jury. Paralysis  may  follow  blows,  cuts  on  the  arm  or  fore- 
arm, dislocation  and  fractures  of  the  humerus  or  clavicle ;  it 
may  be  compressed  by  callus  or  strained  by  continued  or 
sudden  forced  flexion  of  the  forearm  ;  it  may  be;  dislocated 
at  the  elbow  or  be  involved  by  fractures  and  dislocations  at 
the  elbow,  in  the  forearm,  or  at  the  wrist.  Of  the  cases  of 
ulnar  palsy  recently  coming  to  the  Vanderbilt  clinic,  one 
was  caused  by  a  piece  of  steel  hitting  the  inner  side  of  the 
arm,  and  two  by  falls  on  the  elbow.  The  records  of  the 
Vanderbilt  clinic  show  that  of  all  peripheral  paralyses  due 
to  direct  and  immediate  violence,  ulnar  paralysis  is  the  most 


INJURIES   TO   THE    PERIPHERAL   NERVES.  109 

frequent.  Unlike  the  musculo-spiral,  it  is  rarely  the  seat  of 
pressure  or  sleep  palsy. 

The  symptoms  are  chiefly  motor,  and  their  distribution 
may  be  readily  inferred  by  recalling  the  distribution  of  the 
nerve.  Loss  of  power  in  the  flexor  carpi  ulnaris  causes 
weakness  in  flexion  of  the  wrist ;  loss  of  power  in  the  inner 
half  of  the  flexor  profundus  digitorum  causes  weakness  in 
flexion  of  the  two  internal  fingers.  In  complete  ulnar  pa- 
ralysis the  little  finger  can  not  be  moved  at  all. 

The  most  characteristic  and  disabling  effect  of  paralysis 
of  this  nerve  is  paralysis  of  the  interossei,  all  of  which  it 
supplies.  The  interossei  flex  the  first  and  extend  the  second 
and  third  phalanges  of  the  fingers,  which  actions  are  neces- 
sary in  writing  and  in  most  of  the  finer  movements  of  the 
hand.  The  loss  of  them  causes  very  serious  inconvenience. 
The  interossei  also  adduct  and  abduct  the  fingers  and  ad- 
duct  the  thumb,  movements  which  can  no  longer  be  per- 
formed when  the  ulnar  is  paralyzed. 

Atrophy  of  paralyzed  muscles  and  overaction  on  the 
part  of  opposing  muscles  are  early  complications  in  ulnar 
palsy.  In  beginning  stages  the  condition  is  manifested  by 
slight  overextension  of  the  first  phalanges  of  the  fingers, 
especially  the  little  finger  (Fig.  27),  and  an  inability  to 
firmly  extend  the  terminal  phalanges.  If  the  palsy  is 
complete  and  permanent,  the  deformity  becomes  verv 
marked,  constituting  the  claw  hand  or  main  en  griffe  of 
Duchenne. 

The  sensory  distribution  of  the  ulnar  nerve  is  limited  to 
the  inner  side  of  the  anterior  and  posterior  surfaces  of  the 
hand.  Posteriorly  it  extends  a  little  above  the  wrist  and 
includes  part  of  the  dorsal  surface  of  the  middle  finger,  and 
the  ring  and  little  fingers ;  anteriorly  it  is  limited  to  the 
hand  and  two  inner  fingers. 

The  sensory  symptoms  which  occur  as  a  result  of  ulnar 
palsy  are  chiefly  subjective — numbness,  tingling,  and  simi- 


J  JO  ORGANIC   EFFECTS   OF    INJURY. 

lar  sensations.  There  may  be  some  diminution  of  cutane, 
ous  sensibility,  but  complete  ansesthesia  is  extremely  rare, 
unless  the  nerve  is  inflamed  as  well  as  injured.* 

Prognosis. — Ulnar  palsy,  when  it   occurs  as  a  result  of 
pressure  from  dislocated   bones,   usually  recovers  in  a  few 


Fig.  27.— Beginning  main  en  griffe.     From  an  injury  to  the  ulnar  nerve. 
(Almshouse  Hospital.) 

weeks  or  months,  if  the  dislocation  is  reduced  and  if  the 
nerve  is  not  too  seriously  lacerated  or  compressed.  In  frac- 
tures there  is  more  danger  of  the  nerve  being  lacerated,  and 
consequently  the  prognosis  should  be  given  with  greater  re- 

*  The  ulnar  nerve  seems  particularly  liable  to  the  somevk'hat  unusual  affection 
Icnown  as  ascending  neuritis,  or  neuritis  migrans.  In  this  extremely  painful  dis- 
ease a  peripheral  nerve  injury,  with  external  wound,  is  followed  by  extensions  of 
the  paralysis  and  the  pain  up  the  course  of  the  nerve  or  to  other  ner^'es.  In  a 
patient  at  the  Vanderbilt  clinic  an  ulnar  neuritis  developed,  probably  from  a  cut  on 
the  little  finger,  and  eventually  the  nerve  became  paralyzed  for  all  its  functions. 
The  pain  was  intense,  and  the  swollen  nerve  could  be  felt  as  a  round  cord  in  the 
-whole  of  its  peripheral  course. 


INJURIES   TO   THE   PERIPHERAL   NERVES. 


I  I  I 


serve.  If  the  paralysis  be  due  to  pressure  exerted  by  callus, 
operation  will  be  necessary  for  complete  recovery.  Elec- 
trical examination  may  be  found  useful  in  deciding  upon  the 
necessity  for  operation.  From  ordinary  blows  the  nerve 
usually  recovers  perfectly ;  the  prognosis  when  the  nerve 
has  been  divided  is  the  same  as  for  other  nerves. 


Fig.  28. — Distribution  of  the  sensory  nerves  in  the  hand.     (After  Quain.) 

Musculo-Spiral. — The  musculo-spiral  nerve  arises  from 
the  posterior  cord  of  the  brachial  plexus,  and  carries  in  its 
trunk  fibers  from  all  the  nerve  roots  which  form  the  bra- 
chial plexus  wath  the  exception  of  those  from  the  first 
dorsal  and  those  from  the  fifth  cervical.  Fibers  from  the 
fifth  cervical  are  sometimes  included  (Quain).  It  is  prob- 
able that  in  this  nerve,  as  in  many  others,  the  cells  from 
which  the  motor  fibers  of  the  nerve  arise  are  not  limited 


112 


ORGANIC  EFFECTS  OF  INJURY. 


to  the  spinal  cord  segment  from  which  the  nerve  root 
springs,  but  may  come  from  the  anterior  horn  cells  of  any 
one  of  several  segments. 

Its  situation  in  the  axilla  exposes  the  musculo-spiral 
nerve  to  injury;  dislocations,  and  fractures  of  the  humerus 
and  clavicle,  are  frequently  followed  by  paralysis  of  this 
nerve.  In  the  arm  the  most  frequent  cause  of  musculo- 
spiral  palsy  is  pressure,  whether  caused  by  a  crutch  or 
by  weight  of  the  body  during  sleep.  Blows  and  wounds 
to  the  forearm,  also  fractures  of  the  bones,  may  abolish  its 
function.  Musculo-spiral  paralysis  has  also  resulted  from 
falls  on  the  hand  and  from  sudden  and  forcible  extension  of 
the  arm. 

The  symptoms  are  familiar  to  every  physician.  If  the 
nerve  is  injured  in  the  axilla  or  upper  part  of  the  arm,  there 
will  be  paralysis  of  the  triceps  as  well  as  of  the  muscles 
situated  lower  down.  If  the  nerve  is  injured  below  the 
branch  for  the  triceps  that  muscle  will  escape.  The  other 
muscles  involved  are  the  supinators  of  the  arm,  the  exten- 
sors of  the  wrist  and  fingers  and  of  the  thumb. 

Complete  musculo-spiral  paralysis  causes  the  familar 
drop-wrist  (Fig.  29).  When  drop-wrist  continues  for  any 
length  of  time  there  develops  a  prominence  on  the  back 
of  the  hand  due  to  thickening  of  the  tendon-sheaths.  The 
hand  hangs  helpless,  and  all  efforts  on  the  part  of  the  pa- 
tient at  extension  of  the  wrist  or  of  the  first  phalanges  of  the 
fingers  are  ineffectual.  If  the  hand  is  supported,  thus  giv- 
ing a  point  dappui  to  the  interossei,  the  terminal  phalanges 
can  be  extended  and  the  fingers  separated.  The  power  of 
abduction  and  extension  of  the  thumb  is  lost.  It  frequently 
happens  that  the  extensors  are  not  completely  paralyzed  ; 
when  this  is  the  case  the  paralysis  is  least  marked  in  the 
index  and  little  fingers.  Paralysis  of  the  supinators,,  espe- 
cially of  the  supinator  longus,  causes  the  arm  to  pronate 
when  any  efforts  at  flexion  of  the  wrist  or  fingers  are  at- 


INJURIES   TO   THE    PERIPHERAL   NERVES.  113 

tempted.  In  this  way  the  grip  is  very  much  lessened  in 
force.  By  paralysis  of  the  supinator  longus  the  power  of 
flexion  of  the  forearm  is  diminished.  If  the  triceps  is  in- 
volved, extension  of  the  arm  is  impaired  or  lost.  The  meth- 
ods of  examination   for  most  of    these   muscular  functions 


Fig.  29.— Drop-wrist,  from  palsy  of  the  musculo-spiral  nerve.     (Vanderbilt  Clinic.) 

are  obvious.  The  most  satisfactory  test  for  weakness  in  the 
supinator  longus  is  for  the  patient,  with  the  ulnar  side 
of  the  forearm  resting  upon  a  table,  to  attempt  to  raise 
the  forearm  against  the  resistance  of  the  hand  of  the  ex- 
aminer. 

The  sensory  symptoms  of  paralysis  of  this  nerve  a,re 
usually  limited  to  numbness  and  tingling  of  the  radial  side 
of  the  forearm  and  hand  and  of  the  back  and  outer  side  of 
the  arm.      The    extent  of    the   atrophy  depends  upon  the 


114  ORGANIC  EFFECTS  OF  INJURY. 

severity  of  the  injury.  The  electrical  reactions  are  the  same 
as  for  the  other  nerves.  In  the  larger  number  of  cases  the 
injury  is  of  moderate  severity,  and  so  pronounced  reactions 
of  degeneration  rarely  occur. 

The  diagnosis  of  traumatic  musculo-spiral  paralysis  ordi- 
narily presents  no  difficulties  except  when  a  history  of  acci- 
dent is  unsatisfactory.  Then  it  is  well  to  remember  that 
lead  paralysis  is  usually  bilateral,  and  only  exceptionally 
affects  the  supinator  longus  and  extensor  longus  pollicis. 
Also  lead  poisoning  causes  electrical  changes  of  serious  im- 
port. In  progressive  muscular  atrophy  the  paralysis  is 
rarely  complete,  and  its  distribution  is  ulnar  as  well  as  radial. 
In  progressive  muscular  atrophy  the  electrical  reactions  re- 
main for  a  long  time  normal. 

The  prognosis  of  musculo-spiral  paralysis  is  in  general 
very  favorable  ;  unless  the  injury  has  been  unusually  severe, 
recovery  is  the  rule. 

Combined  Paralyses  of  the  Upper  Extremity. 

Blows  or  falls  on  the  neck  or  shoulder  or  arm,  and  dislo- 
cations and  fractures  of  any  of  the  bones  of  the  upper  ex- 
tremities, may  cause  paralysis  in  more  than  one  nerve. 

Thus  a  patient  came  to  the  Vanderbilt  clinic  with  paraly- 
sis of  the  musculo-spiral,  median,  and  ulnar  nerves,  which 
came  on  immediately  after  a  fall  on  the  palm  of  the  hand. 

The  musculo-spiral  and  ulnar  are  the  nerves  most  fre- 
quently involved  together  in  injuries  around  the  shoulder 
joint,  although  paralysis  of  the  circumflex,  or  the  median  or 
the  musculo-cutaneous,  may  be  added.  The  symptoms  of 
these  combined  paralyses  are  the  sum  of  the  symptoms  of 
lesions  of  the  individual  nerves.  They  are  usually  the 
result  of  severe  injuries,  and  the  prognosis  is  accordingly 
serious.  * 

Injuries  to  the  neck,  falls  upon  the  point  of  the  shoulder, 
and  less  frequently  dislocations  of  the  shoulder,  sometimes 


COMBINED    PARALYSES   OF   THE    UPPER    EXTREMITY,     nj 

cause  a  peculiarly  distributed  paralysis,  first  described  by 
Erb,  and  often  called  Erb's  palsy.  The  muscles  most  fre- 
quently affected  are  the  deltoid,  biceps,  brachialis  anticus, 
and  supinator  longus.  In  several  of  the  Vanderbilt  clinic 
cases  the  supra  and  infra-spinati  were  involved  as  well. 
In  these  cases  there  is  slight  inward  rotation  of  the  arm. 
All  these  muscles,  except  the  last  two,  receive  their  inner- 
vation through  the  fifth  and  sixth  cervical  nerve  roots.  The 
suprascapular  nerve,  which  supplies  the  supra-  and  infra- 
spinati  muscles,  receives  some  fibers  from  the  fourth  cer- 
vical segment,  but  most  of  its  fibers  come  from  the  fifth  and 
sixth  nerve  roots,  and  so  it  may  easily  be  injured  when 
those  roots  are  affected. 

Hoedemaker  has  suggested  that,  in  injuries  to  the  shoul- 
der, paralysis  of  these  nerves  may  occur  by  the  fifth  and 
sixth  nerve  roots  being  compressed  between  the  transverse 
processes  of  the  sixth  and  seventh  cervical  vertebras  and  the 
middle  of  the  clavicle. 

In  cases  where  the  paralysis  is  severe  this  affection  is 
very  disabling.  The  arm  can  not  be  raised  from  the  side, 
and  the  forearm  can  not  be  flexed  or  strongly  rotated  out- 
ward. From  paralysis  of  the  deltoid  the  shoulder  of  the 
affected  side  is  lower  than  its  fellow,  and  there  may  be  a 
slight  subglenoid  dislocation  of  the  humerus.  Atrophy  is 
often  an  early  symptom,  and  there  is  usually  marked  fibril- 
lary twitching  in  the  muscles,  when,  if  not  completely  par- 
alyzed, they  are  put  in  action. 

The  sensory  symptoms  are  never  prominent;  there  may 
be  numbness  and  tingling  in  the  region  of  the  shoulder,  or 
in  the  radial  distribution  of  the  forearm  and  hand.  The 
electrical  reactions  soon  show  degenerative  changes. 

All  these  muscles  may,  in  health,  be  made  to  contract  by 
applying  the  electric  current  at  a  point  in  the  neck  called 
Erb's  point  (see  Fig.  7);  after  injury  disordered  electrical 
reactions  soon  become  manifest  at  this  same  point.     A  Van- 


Il6  ORGANIC  EFFECTS  OF  INJURY. 

derbilt  clinic  case  after  a  fall  on  the  right  shoulder  com- 
plained of  some  weakness  in  the  shoulder  muscles  of  that 
side,  especially  in  the  morning.  The  man  was  left-handed, 
and  examination  showed  only  a  comparative  weakness  of 
the  right  deltoid,  biceps,  and  supinators.  This  weakness 
might  have  been  a  normal  difference  between  the  right  and 
left  side,  and  the  diagnosis  was  not  clear.  But  when  the 
galvanic  response  in  these  muscles,  obtained  through  Erb's 
point,  was  found  considerably  exaggerated  on  the  right  side, 
it  became  evident  that  the  patient  was  suffering  from  a  very 
mild  injury  to  the  upper  part  of  the  brachial  plexus. 

The  diagnosis  of  this  affection  is  extremely  simple  if 
the  patient  is  examined  for  muscular  power  and  by  elec- 
tricity. In  severe  cases,  in  which  the  deltoid  is  so  re- 
laxed that  it  permits  a  slight  subglenoid  dislocation  of  the 
shoulder,  the  condition  is  sometimes  mistaken  for  a  simple 
dislocation.  Such  errors  are  the  results  of  superficial  ex- 
amination. 

The  general  prognosis  of  this  form  of  paralysis  is  good, 
in  that  the  patients  usually  recover.  In  my  experience, 
however,  such  recovery  has  always  been  tedious,  extending 
over  man}^  months. 

Another  form  of  brachial-plexus  paralysis  involves  the 
first  anterior  dorsal  root.  Through  this  root  pass  the  sym- 
pathetic fibers  for  the  eye.  The  condition  was  first  thor- 
oughly studied  by  Klumpke,  and  is  called  Klumpke's,  or 
the  lower  arm  tvpe  of  brachial-plexus  palsy.  It  consists  in 
a  paralysis  of  the  small  muscles  of  the  hand,  and  evidences 
of  disturbance  of  the  sympathetic  on  the  same  side  of  the 
face.  There  are  myosis,  diminished  palpebral  fissure,  loss 
of  the  cilio-spinal  reflex,  sinking  in  of  the  eye,  and  flatten- 
ing of  the  face.  There  are  no  vaso-motor  disturbances. 
Klumpke's  paralysis,  as  an  isolated  paralysis  of  the  brachial 
plexus,  is  a  great  rarity.  It  occurs  from  causes  similar  to 
those  already  mentioned   in   lesions  affecting  the  fifth  and 


COMBINED   PARALYSES   OF   THE    UPPER   EXTREMITY,    ny 

sixth  cervical  roots,  causing  Erb's  palsy.  The  lower  roots 
of  the  brachial  plexus  are  affected  much  less  frequently, 
however,  than  the  upper,  and  Klumpke's  paralysis  is  much 
more  uncommon  than  the  variety  named  after  Erb. 

Klumpke's  paralysis  is  only  infrequently  seen  in  its  pure  form. 
It  is  usually  more  comprehensive,  and  differs  in  other  ways  from  the 
variety  of  brachial  plexus  lesion  first  described  by  that  observer. 
Thus,  in  a  case  at  the  Vanderbilt  clinic,  a  man  fell  on  the  right 
:shoulder,  fracturing  the  clavicle.  After  the  bone  lesion  had 
healed  the  patient  presented  the  following  symptoms  :  Left  myo- 
sis  without  other  evidences  of  sympathetic  disturbances;  difficulty 
in  raising  and  flexing  the  arm,  and  an  almost  total  disability  in 
performing  the  finer  movements  of  the  fingers  and  in  flexing  the 
wrist  and  hand.  There  was  slight  anaesthesia  along  the  inner  side 
of  the  arm.  The  deltoid  and  biceps  reacted  to  faradism,  but  the 
muscles  supplied  by  the  median  and  ulnar  nerves  presented  de- 
generative electrical  reactions.  Thus  in  this  case  myosis  was  the 
only  evidence  of  disturbance  of  the  sympathetic,  but  in  addition 
to  palsy  of  the  circumflex  and  musculo-cutaneous  nerves  there 
ivas  affection  of  the  median  and  ulnar. 

The  paralyses  of  the  lumbar  and  sacral  plexuses  are  rela- 
tively infrequent,  and  result  from  causes  similar  to  those 
enumerated  for  the  palsies  of  the  arm.  When  traumatic, 
they  are  usually  the  results  of  fractures  or  dislocations  of  the 
lumbar  vertebrae  or  of  the  pelvis.  It  may  be  sufficient  to 
recall  that  the  lumbar  plexus  supplies  the  muscles  concerned 
in  flexion  and  adduction  of  the  thigh,  and  to  a  slight  extent  in 
rotation  outward,  and  in  extension  of  the  leg.  Consequently 
the  knee-jerk  may  be  lost  in  paralysis  of  the  lumbar  plexus. 
The  other  muscles  of  the  hip  and  thigh,  and  all  the  muscles 
of  the  leg,  receive  their  innervation  through  the  sacral  plexus. 

Injuries  to  the  lumbar  or  sacral  plexus,  or  to  any  of 
their  ultimate  branches,  are  followed  by  the  same  kind  of 
symptoms  as  have  been  described  under  the  palsies  of  the 
cervical  and  brachial  plexus,  and  may  easily  be  diagnosti- 
•cated  by  remembering  the  distribution  of  the  nerves. 

9 


jjg  ORGANIC  EFFECTS  OF  INJURY. 

Bibliography. 

Bernhardt,  Die  Erkrankungen  der  Peripherischen  Nerven. 
Nothnagel's  Spec.  Path.  u?id  Therapie,  Wien,  1895. 

Hoedemaker,  Ueber  die  von  Erb  zuerst  beschreiben  combinirte 
Lahmungsform  an  der  oberen  Extremitat.  Arch,  fur  Psych., 
1879,  ix,  p.  738. 

Howell  and  Huber,  A  Physiological,  Histological,  and  Clinical 
Study  of  the  Degeneration  and  Regeneration  in  Peripheral  Nerve 
Fibers  after  Severance  of  their  Connection  with  the  Nerve  Cen- 
ters.    J  our  7ial  of  Physiology,  1892,  xiii.  No.  5  ;   1893,  xiv,  No.  i. 

Gowers,  Diseases  of  the  Nervous  System,  second  edition,  Lon- 
don, 1893. 

Klumpke,  Contribution  a  I'etude  des  paralysies  radiculaires  da 
plexus  brachial.     Revue  de  7/ied.,  1885,  No.  7. 

Litten,  Ueber  die  normaliter  bei  jeder  Respiration  am  Tho- 
rax sichtbaren  Zwerchfellbewegungen.  Deut.  vied.  Woch.,  1892,. 
No.  13. 

Mitchell,  J.  K.,  Remote  Consequences  of  Injuries  of  Nerves. 
Philadelphia,  1894. 

Mitchell,  S.  Weir,  Injuries  of  Nerves  and  their  Consequences. 
Philadelphia,  1872. 

Quain,  The  Nerves.     London,  1895. 

Stroebe,  Die  allgem.  Histol.  der  degenerativ  u.  regener.  Pro- 
cesse  im  central,  u.  periph.  Nervensystem.  Cblatt.  fUr  allg.  Path, 
und path.  Anat.,  i?>()^-q6,  p.  849. 


CHAPTER   IV. 

ULTIMATE   ORGANIC   EFFECTS   OF   INJURY. 

While  the  exact  diagnosis  of  the  acute  conditions  which 
have  been  described  in  the  preceding  pages  sometimes  pre- 
sent difficulties,  their  aetiology  is  in  most  cases  easy  of  dem- 
onstration. 

When  an  organic  injury  is  immediately  followed  by 
symptoms  of  well-recognized  pathological  conditions  in  the 
nervous  system  there  is  rarely  any  question  as  to  the  pro- 
priety of  associating  the  two  occurrences  in  the  direct  re- 
lationship of  cause  and  effect.  The  ultimate  termination  de- 
pends upon  the  nature  of  the  injury  and  upon  the  part  of 
the  nervous  system  which  has  been  affected  by  it.  It  is 
often  difficult  to  foresee  what  this  termination  is  to  be. 

Of  cerebral  lesions  the  possible  variety  of  final  results  is 
almost  unlimited.  Death  may  ensue  instantly  or  after  vary- 
ing periods  of  time,  and  may  be  due  to  the  destruction  of 
vital  centers ;  or  the  lesion  of  the  brain  may  be  the  one  addi- 
tional straw  which  an  already  enfeebled  constitution  is  un- 
able to  carry.  If  the  patient  lives  he  may  recover  from  the 
immediate  effects  of  the  injury,  but  may  remain  perma- 
nently paralyzed  as  regards  motion  or  special  sense  func- 
tion, or  be  left  with  a  serious  and  incurable  impairment  of 
the  intellectual  faculties.  Dementia,  associated  or  not  with 
paralysis,  is  one  of  the  most  frequent  of  the  permanent  re- 
sults of  severe  injuries  to  the  brain. 

This  is  illustrated  by  a  man  at  present  under  my  observation, 
who  at  the  time  of  the  accident  was  under  the  care  of  Dr.  Bolton 


I20  ORGANIC   EFFECTS   OF   INJURY. 

at  the  Hudson  Street  Hospital.  The  patient  was  a  fireman,  thirty- 
one  years  of  age,  who  fell  through  a  hatchway,  striking  on  his 
head  and  fracturing  his  skull.  When  brought  to  the  hospital  he 
was  in  a  stupor,  was  very  irritable  and  noisy,  and  presented  evi- 
dences of  paralysis  of  the  left  arm  and  left  leg,  and  of  ptosis  on 
the  right  side. 

The  physical  symptoms  disappeared  in  a  few  weeks,  but  al- 
though it  is  now  several  months  since  the  accident,  and  although 
he  has  regained  good  general  health,  the  patient  remains  slovenly, 
unable  to  care  for  himself,  or  to  talk  intelligibly  or  to  understand 
what  is  said  to  him.  He  sits  quietly  in  his  chair,  oblivious  to  his 
surroundings,  and  though  able  to  perform  all  movements  perfectly 
well,  he  does  not  move  unless  told  to  do  so.  He  is  at  present 
completely  demented,  and  hopes  for  his  recovery  do  not  seem 
bright. 

Any  of  the  psychoses  may  develop  after  severe  injuries 
to  the  head,  w^hether  the  skull  has  or  has  not  been  fractured. 
Mania  and  melancholia  are  the  most  common  of  the  trau- 
matic psychoses.  They  may  appear  weeks  or  months  after 
the  accident,  and  usually  present  no  symptomatic  differences 
from  like  psychoses  of  idiopathic  origin.  Their  prognosis 
is  always  grave,  although  some  cases,  in  which  there  was 
a  depressed  fracture  of  the  skull,  have  been  benefited  by 
operation.  Neurasthenia  and  hysteria  may  also  be  the  re- 
sult of  severe  injuries  to  the  head,  although  these  disorders 
more  commonly  follow  accidents  of  less  gravity. 

It  is  often  impossible  in  an  individual  case  to  foresee 
what  the  ultimate  effects  of  severe  head  injuries  are  to  be. 
In  the  cases  in  which  the  evidences  of  extensive  hemorrhage 
or  laceration  of  the  brain  are  pronounced  it  is  usually  ap- 
parent that  the  patient  has  not  long  to  live ;  but  when  the 
symptoms  do  not  unequivocally  point  to  a  fatal  lesion  there 
are  no  means  by  which  it  may  be  foretold  how  complete 
recovery  is  to  be  or  if  it  is  to  occur  at  all.  Abscess  of  the 
brain  may  develop  after  injuries  to  the  head  in  which  the 
only  immediate  symptoms  were  scalp  wounds  or  in  which 
any  abrasion  in  the  cranial  covering  was  not  discoverable. 


ULTIMATE   ORGANIC    EFFECTS   OF    INJURY.  121 

In  acute  traumatism  of  the  spinal  cord  the  prognosis  is 
bad,  both  as  to  life  and  as  regards  recovery.  Lesions  of 
spinal-cord  structure  are  irreparable  ;  if  nerve  fibers  or 
nerve  cells  are  destroyed,  they  are  not  replaced.  The  only 
hope,  in  cases  of  traumatic  paraplegia,  that  the  symptoms 
may  entirely  disappear,  depends  upon  the  loss  of  function 
being  due  to  some  lesion  such  as  extrameduUary  haemor- 
rhage, which  temporarily  abolishes  function  v^ithout  seri- 
ously disturbing  structure.  When  the  cord  is  completely 
cut  across  there  is  no  chance  for  recovery,  and  the  patient 
usually  dies  in  a  few  days  as  a  result  of  the  injury.  In 
many  cases  the  lesion  is  not  completely  transverse,  and  the 
patients  regain  a  certain  amount  of  muscular  power,  and 
control  of  the  sphincters  may  be  restored.  Anaesthesia  fre- 
quently disappears  almost  entirely.  In  general,  any  one 
who  sustains  an  injury  to  the  spinal  cord,  if  he  does  not 
die,  remains  more  or  less  of  a  cripple  for  life,  although  this 
rule  has  its  exceptions.  The  nearer  to  the  brain  the  lesion 
is  situated  the  worse  is  the  prognosis  for  life.  Injuries  to 
the  fourth  cervical  segment,  or  to  segments  above  it,  are 
almost  immediately  fatal.  The  mortality  of  all  cervical 
lesions  is  very  high.  The  prognosis  is  somewhat  better 
when  they  are  in  the  dorsal  region,  and  is  most  favorable 
for  those  of  the  lumbo-sacral  region  and  of  the  cauda  equina. 

When  there  is  a  time  interval  between  the  receipt  of  any 
injury  to  the  nervous  system  and  the  appearance  of  the 
symptoms  which  may  be  alleged  to  be  its  direct  result,  a 
causal  connection  is  much  more  difificult  of  proof.  The 
question  of  the  traumatic  origin  of  tumors  of  the  nervous 
system  is  even  more  obscure  than  when  new  growths  de- 
velop in  other  parts  of  the  body  apparently  as  the  direct 
consequence  of  injury.  According  to  the  theory  of  Cohn- 
heim,  tumors  have  their  origin  in  undeveloped  embryonal 
cells  which  remain  inactive  until,  through  the  agency  of 
some  exciting  cause,  they   are   stimulated   to  a  disordered 


J 22  ORGANIC   EFFECTS   OF    INJURY. 

growth.  The  nature  of  the  essential  exciting  causes  is  un- 
known, but  that  trauma  is  one  of  them  is  commonly  be- 
lieved. There  is  little  question  as  to  the  possibility  of 
long-continued  irritation  inducing  malignant  neoplasms, 
especially  in  the  mucous  membranes.  To  prove  that  a 
single  acute  injury  may  bring  about  such  a  result  is  very 
much  more  difficult.  As  far  as  the  nervous  system  is  con- 
cerned, the  evidence  for  the  traumatic  origin  of  tumors  can 
not  be  regarded  as  anything  more  than  suggestive. 

Thus  in  a  recent  autopsy  held  at  the  Almshouse  upon  the 
body  of  a  woman,  seventy-one  years  of  age,  who  had  never  given 
any  symptoms  of  cerebral  disturbance,  there  was  found  a  large 
endothelioma  upon  the  internal  surface  of  the  dura  mater,  on  the 
right  side  of  the  middle  fossa  of  the  skull,  lying  adjacent  to  the 
squamous  portion  of  the  temporal  bone  just  posteriorly  to  the 
greater  wing  of  the  sphenoid.  On  the  opposite  side  of  the  skull 
was  an  old,  undepressed  fracture.  The  question  is  of  course  open 
as  to  whether  the  situation  of  the  tumor  were  entirely  accidental, 
or  whether  at  the  time  of  the  fracture  sufficient  force  was  exerted 
by  contrecoup  to  incite  to  morbid  activity  embryonal  cells  in  the 
dura  mater,  with  the  resulting  formation  of  an  endothelioma. 

A  still  more  suggestive  case  has  been  reported  by  Carara*  in 
which  a  man,  previously  well,  received  a  blow  on  the  head  and  died 
of  tumor  of  the  brain  within  five  months.  The  patient,  who  was 
thirty-nine  years  of  age,  was  struck  with  a  stick  on  the  left  pos- 
terior parietal  region.  The  scalp  wound  healed  in  about  six 
weeks,  but  there  soon  occurred  headache,  deafness  in  the  left  ear, 
and  dizziness  and  numbness  of  the  left  side.  These  symptoms  be- 
came worse,  and  the  patient  entered  the  hospital,  where  it  was 
found  that  in  addition  to  the  symptoms  already  mentioned  there 
were  a  weakness  and  diminution  of  cutaneous  sensibility  in  the  left 
arm  and  leg.  The  reflexes  were  normal.  The  patient  began  to  have 
convulsive  seizures,  and  soon  after  this  he  died.  The  autopsy 
showed  that  the  skull  was  not  fractured,  but  that  there  was  a 
glioma  in  the  right  side  of  the  brain,  in  the  neighborhood  of  the 
Rolandic  fissure.  Whatever  may  be  one's  opinion,  it  is  impossible 
to  decide  whether  the  blow  on  the  head  was  the  sole  cause,  or 
whether  the  tumor  had  begun  to  grow  before  it  was  received. 


*  Vierteljahrschrift  fiir  gerichtliche  Medicin,  January,  1896. 


ULTIMATE   ORGANIC   EFFECTS   OF    INJURY.  123 

According  to  views  recently  expressed  by  Striimpell  * 
as  to  the  pathology  of  multiple  sclerosis,  the  genesis  of  that 


Fig.  30. — Deformity  of  the  back  caused  by  syringomyelia.     (Vanderbilt  clinic.) 

■disease  depends  upon  a   nT.orbid  activity  being  given  to  ab- 
normal islets  of  neuroglia  tissue  scattered  throughout  the 


*  Neurologische  Centralblatt,  1896,  No.  21. 


124  ORGANIC   EFFECTS   OF    INJURY. 

cerebro-spinal  axis.  If  this  theory  is  correct,  the  setiology 
of  multiple  sclerosis  is  probably  similar  to  that  of  tumors ;. 
yet  clinical  substantiation  that  multiple  sclerosis  arises  from 
traumatic  causes  is  still  slight.  This  subject  will  again  be 
referred  to. 

So  little  is  known  about  the  pathology  of  acromegaly 
(Fig.  31),  and  the  disease  is  itself  so  rare,  that  knowledge  of 
the  part  played  by  injury  in  its  causation  is  still  largely 
speculative.  Unverricht,  *  however,  describes  a  case  of 
typical  acromegaly  in  a  patient  who  had  received  an  injury,, 
and  whom  the  examining  physician  had  regarded  first  as  a 
simulator  and  later  as  an  example  of  "  traumatic  neurosis." 
Unverricht  adduces  several  other  cases  of  alleged  traumatic 
origin. 

The  relationship  of  traumatism  to  diseases  of  the  nerv- 
ous system  is  necessarily  so  obscure  that  it  can  not  be  even 
approximately  decided  except  for  those  disorders  which  are 
comparatively  frequent.  Thus,  although  there  is  no  doubt 
but  that  spinal  haemorrhage  may  give  rise  to  conditions  in 
the  spinal  cord  similar  to  those  found  in  syringomyelia, 
there  is  as  yet  only  very  meager  clinical  evidence  for  the 
existence  of  traumatic  syringomyelia. 

Laehrf  reports  two  cases,  in  each  of  which  the  disease- 
already  existed  at  the  time  of  the  injury,  and  Huisman  +  has 
recently  described  as  traumatic  a  case  in  which  the  relation- 
ship of  the  injury  to  the  spinal  disease  is  not  clear.  A  simi- 
lar uncertainty  exists  in  regard  to  the  traumatic  aetiology  of 
ataxic  paraplegia  and  chronic  progressive  spastic  paraplegia.. 

TJiere  is,  however,  a  group  of  comparatively  common 
chronic  degenerative  diseases  of  the  nervous  system  of 
which  traumatism  is  regularly  spoken  of  as  a  cause,  and 
which,  by  reason  of  the  symptoms  being  often  observed  for 

*  Miinchener  medicinische  Wochenschrift,  1895,  xlii,  14. 

f  Char.  Annalen,  1895,  Jahrg.  xx. 

\  Deutsche  medicinische  Wochenschrift,  February,  1897.. 


ULTIMATE   ORGANIC    EFFECTS   OF    INJURY. 


125 


the  first  time  after  some  accident,  have  important  forensic 
relations.  These  diseases  are  epilepsy,  general  paralysis  of 
the  insane,  locomotor  ataxia,  progressive  muscular  atrophy,  and 
paralysis  agitans.      In  some   of   them   the  occasional  occur- 


FiG.  31.— Acromegaly.     (Photograph  of  a  female  patient  who  died  in  the 
Incurable  Hospital.) 


rence  of  trauma  as  a  sole  cause  seems  probable;  In  others 
the  possibility  of  a  traumatic  origin  is  extremely  doubtful, 
as  is  indicated  by  the  absence  of  well-authenticated  cases 
which  have  occurred  in  this  way.  Epilepsy  is  the  only  one 
of  the  group  which  can  be  positively  proved,  both  clinically 
and  pathologically,  to  owe  its  development,  in  certain  cases, 
solely  to  trauma. 

So  many  factors  must  be  taken  into  account  in  a  consid- 


126  ORGANIC  EFFECTS  OF  INJURY. 

eration  of  these  diseases  and  their  relationship  to  injury  that 
they  require  individual  description. 

Epilepsy. 

Epilepsy  is  one  of  the  most  frequent  affections  of  the 
nervous  system,  and  is  among  the  commonest  of  chronic 
diseases.  It  is  estimated  as  occuring  in  one  of  every  five 
hundred  of  the  population.  In  the  larger  number  of  cases 
no  cause  can  be  found  to  explain  the  convulsions ;  then  the 
epilepsy  is  called  idiopathic  and  is  regarded  as  a  disease 
sui  generis.  In  a  small  percentage  of  the  total  number  of 
cases  the  convulsions  can  be  shown  to  depend  upon  gross 
intracranial  lesions  (Jacksonian  epilepsy)  or  upon  the  irri- 
tation of  the  cortical  cells  by  toxic  substances  circulating 
in  the  blood.  In  such  cases  the  convulsions  are  the  expres- 
sions of  definite  pathological  states. 

When  the  attacks  occur  as  the  immediate  result  of  phys- 
ical injury,  epilepsy  is  called  traumatic ;  the  trauma  causes 
some  morbid  alterations  in  the  brain  substance  which  find 
their  clinical  expressions  in  recurring  convulsions. 

The  frequency  of  traumatic  epilepsy,  as  compared  with 
the  idiopathic  form,  is  somewhat  difihcult  to  determine.  If 
we  are  to  accept  as  traumatic  every  case  which  has  the  his- 
tory of  a  fall,  or  a  blow  on  the  head,  received  years  before 
the  appearance  of  convulsions  which  are  from  the  first  gen- 
eral in  character,  the  category  of  idiopathic  epilepsy  would 
become  very  restricted  ;  for  few  persons  reach  adolescence 
without  *a  fall  or  an  injury  of  some  kind,  and  almost  every 
epileptic  patient  can  be  made,  if  closely  questioned,  to  admit 
some  such  history.  According  to  the  books  at  the  Vander- 
bilt  clinic,  a  large  percentage  of  all  the  patients  had  falls  in 
infancy,  or  frights,  or  other  trivial  traumatisms,  but  they  are 
not  regarded  as  examples  of  traumatic  epilepsy,  and  it  seems 
doubtful  if  even  one  per  cent  of  the  total  number  of  cases  of 
the  disease  could  be  proved,  with  reasonable  probability,  to 


EPILEPSY.  ■  127 

have  been  the  direct  result  of  injury.  But  whatever  the 
true  cause  of  epilepsy  may  eventually  be  shown  to  be,  our 
actual  knowledge  permits  us  to  recognize  as  traumatic  only 
such  cases  as  develop  within  a  reasonable  length  of  time 
after  a  severe  injury,  or  as  indicate  by  their  symptoms  that 
there  has  been  an  injury  to  a  limited  portion  of  the  brain. 

Our  knowledge  of  the  patJiology  of  traumatic  epilepsy  is 
much  more  definite  than  that  of  the  idiopathic  form.  It  has 
been  carefully  studied  by  Van  Gieson.  There  is  frequently 
a  fracture  of  the  skull,  so  that  splinters  of  bone  press  upon 
the  cortex;  or  without  fracture  there  may  be  an  exostosis 
beneath  the  site  of  the  original  injury.  The  membranes  may 
be  adherent  to  one  another,  and  thus  form  the  starting  point 
of  wedges  of  connective  tissue  which  grow  downward  at 
the  expense  of  brain  tissue.  The  nerve  cells  in  the  affected 
area  are  found  in  various  degrees  of  degeneration,  or  they 
may  have  entirely  disappeared,  having  been  replaced  by 
islets  of  neuroglia  which  have  developed  in  the  course  of 
the  arteries  that  pass  perpendicularly  from  the  surface  into 
the  brain  cortex.  These  morbid  changes  are  fairly  constant 
in  traumatic  epilepsy,  and  are  sufficient  to  permit  the  disease 
to  be  regarded  as  due  to  organic  cerebral  lesion  ;  but  in 
furnishing  a  pathological  anatomy  they  do  not  explain  the 
paroxysmal  nature  of  the  symptoms.  If  the  cerebral  lesion 
is  sufficient  *to  cause  paralysis,  that  symptom  can  very  easily 
be  understood  by  remembering  that  injury  to  the  cortex  has 
injured  or  killed  the  cells  which  are  the  essential  factors  in 
voluntary  motion.  But  why  cells,  whether  they  clo  or  do 
not  retain  the  power  of  causing  voluntary  movement,  should 
from  time  to  time  become  the  seat  of  irritation  and  thus 
cause  convulsions,  remains  unexplained. 

iEtiology. — In  the  aetiology  of  traumatic  epilepsy  pre- 
disposition plays  a  subsidiary  role.  General  convulsions 
sometimes  develop  soon  after  a  slight  injury  to  the  head  or 
to  other  parts  in  persons  who  are  hereditarily  neurotic,  or 


128  ORGANIC   EFFECTS   OF   INJURY. 

whose  nervous  systems,  as  a  result  of  alcoholism  or  other 
forms  of  chronic  poisoning-  or  degeneration,  have  become 
less  resistant  to  injurious  influences  or  stimuli.  In  such 
cases  it  is  often  impossible  to  determine  the  causal  value  of 
the  injury.  The  general  character  of  the  convulsions  would 
seem  to  indicate  that  no  one  portion  of  the  brain  had  been 
traumatized,  but  that  the  whole  cerebral  cortex  was  in  a 
condition  of  latent  disease  that  required  only  a  slight  dis- 
turbance of  the  cerebral  equilibrium  to  become  active.  We 
must  know  very  much  more  about  cerebral  pathology  than 
we  do  at  present  before  it  will  be  possible  to  decide  whether 
such  cases  can  properly  be  regarded  as  the  direct  results  of 
injury,  or  whether  epilepsy  would  have  eventually  devel- 
oped as  a  consequence  of  some  one  of  the  mishaps  of  daily 
life  to  which  every  one  is  exposed. 

Of  the  immediate  causes  of  the  disease,  injuries  to  the 
head  are  the  most  important.  The  records  of  the  Franco- 
Prussian  War  show  that  from  8,985  head  injuries  there  devel- 
oped 46  cases  of  epilepsy.  The  same  records  show  17  cases 
among  77,461  persons  wounded  in  the  body  or  extremities. 
Thus  head  injury  is  not  everywhere  regarded  as  the  sole 
cause. 

It  seems,  however,  extremely  improbable  that  wounds  or 
injuries  by  which  the  brain  is  unaffected,  occurring  to  per- 
sons who  were  not  already  doomed  to  present  manifesta- 
tions of  the  disease,  can  be  regarded  as  causes  of  epilepsy. 
At  the  Vanderbilt  chnic,  among  the  records  of  over  one 
thousand  cases,  injury  to  the  head  is  the  sole  form  of  phys- 
ical traumatism  which  has  been  alleged  as  active  in  the  pro- 
duction of  the  disorder.  It  is  possible  that  injuries  to  other 
parts  may  be  followed  by  epilepsy,  as  injury  may  be  followed 
by  any  disease,  but  in  such  cases  the  influence  of  the  trauma- 
tism must  be  regarded  as  inconsequential. 

As  regards  epilepsy,  severity  is  the  most  important  ele- 
ment of  a  head  injury.     Blows  on  the  head  with  clubs  or 


EPILEPSY. 


129 


heavy  instruments,  striking  the  head  in  falls  or  in  other 
ways,  are  not  uncommonly  followed  by  the  disease.  In 
most  of  the  cases  the  skull  is  fractured,  either  in  the  internal 
or  external  table,  so  that  the  brain  is  directly  pressed  upon. 
But  in  some  cases  Jacksonian  epilepsy  apparently  develops 
as  a  result  of  an  injury  to  the  head  which  has  not  fractured 
the  bone. 

Thus  in  a  case  reported  by  Lloyd  and  Deaver,  the  patient  was 
struck  on  the  right  side  of  the  head  at  the  age  of  sixteen  ;  five 
years  afterward  he  began  to  have  fits,  which  commenced  with 
numbness  and  spasm  in  the  left  arm,  extending  to  the  left  side  of 
the  face;  consciousness  was  not  often  lost  during  the  attack.  The 
skull  was  trephined  over  the  hand  and  arm  center;  there  was  no 
fracture,  and  the  brain  and  meninges  appeared  normal. 

Similarly,  in  a  case  of  Starr's,  the  patient  was  hit  on  the  left 
side  of  the  head  with  a  sand-bag,  and  was  rendered  unconscious 
for  twelve  days.  The  skull  was  not  fractured,  as  was  proved  by 
operation,  but  in  three  months  the  patient  began  to  have  attacks 
of  aphasia  and  convulsions  in  the  right  hand. 

Interval. — The  fits  may  ensue  almost  immediately,  or 
may  be  separated  from  the  occurrence  of  the  original  injury 
by  a  period  often  varying  from  months  to  years. 

Thus  in  a  case  of  Starr's,  a  boy  eighteen  years  old,  previously 
healthy,  received  a  traumatism  of  the  right  parietal  bone  by  being 
struck  on  the  head  by  a  heavy  block  of  wood.  In  three  weeks  he 
began  to  have  frequent  attacks,  which  were  characterized  at  first 
by  tingling  and  numbness  in  the  left  hand,  a  sensation  which  ex- 
tended up  the  arm  to  the  shoulder,  and  then  down  the  trunk  and 
leg,  never  involving  the  face.  The  subjective  sensations  were 
followed  by  twitching  of  the  muscles  of  the  arm  without  involving 
other  parts  and  without  being  accompanied  by  loss  of  conscious- 
ness. The  attacks  lasted  about  a  minute,  and  between  them  there 
was  neither  paralysis  nor  anaesthesia.  It  was  not  possible  to  deter- 
mine by  palpation  of  the  scalp  whether  the  bone  was  fractured  or 
not;  but  an  operation  showed  that  there  was  a  linear  fracture  of 
the  right  parietal  bone,  and  that  immediately  over  the  hand  center 
there  was  imbedded  in  the  dura  a  splinter  of  bone  one  inch  long 
and  three  quarters  of  an  inch  wide. 


I^o  ORGANIC   EFFECTS   OF   INJURY. 

In  contrast  to  this  case,  which  developed  so  quickly,  is 
another  one,  equall}'  typical  of  traumatic  epilepsy,  but  in 
which  the  fits  did  not  appear  until  three  years  after  the 
accident. 

A  man,  twenty-four  years  of  age,  sustained  a  fracture  of  the 
skull  on  the  right  side  about  the  middle  of  the  coronal  suture. 
He  recovered  from  the  acute  effects  of  the  injury,  but  three  years 
later  began  to  have  epileptic  attacks.  The  fits  began  with  a 
movement  of  the  left  hand  and  v/ith  a  turning  of  the  head  to  the 
left ;  the  patient  then  lost  consciousness,  and  the  convulsion  be- 
came general.  Operation  over  the  right  arm  center  showed  that 
a  splinter  of  bone  was  indenting  the  dura,  that  the  dura  was  thick- 
ened, and  that  the  brain  was  yellower  and  more  oedematous  than 
usual. 

Many  cases  have  been  reported  as  traumatic  in  which  the 
time  elapsing  between  the  occurrence  of  the  injury  and  the 
first  appearance  of  convulsions  has  been  much  longer,  being 
five  or  ten  or  even  a  greater  number  of  years.  In  such  cases, 
inasmuch  as  the  fits  are  almost  always  general,  it  is  more 
difficult  to  prove  the  causal  relationship  of  the  traumatism 
to  the  convulsive  symptoms.  So  long  an  interval,  however, 
is  unusual.  Of  forty-four  cases  of  traumatic  epilepsy  which 
were  operated  upon  (collected  by  Mason  for  Gray),  most  of 
the  fits  began  in  a  few  weeks  or  months  after  the  injury. 
Five  cases  appeared  after  an  interval  ranging  from  three 
and  a  half  to  fourteen  years,  but  in  all  of  these,  except  one, 
the  convulsions  were  general  and  the  influence  of  the  trau- 
matism consequently  obscure.  The  exception  is  the  case 
of  Lloyd  and  Deaver,  to  which  reference  has  already  been 
made. 

In  the  interval  between  the  accident  and  the  appearance 
of  the  first  fit  the  patient  may  be  perfectly  well  after  recov- 
ery from  the  acute  effects  of  the  injury.  If  the  motor  tract 
has  been  directly  injured,  there  may  be  hemiplegia  ;  or  if  the 
dura  has  been  irritated,  there  may  be  the  headaches  charac- 
teristic of  pachymeningitis. 


EPILEPSY. 


131 


Thus  a  patient  at  the  Vanderbilt  clinic,  previously  healthy  and 
without  nervous  predisposition,  when  a  boy  of  eleven  years  of  age 
was  thrown  from  a  wagon,  striking  his  head.  Since  that  time  he 
has  had  severe  generalized  headaches  and  petit  mal  attacks,  both 
of  which  later  became  frequent.  The  physical  examination  was 
negative.  There  were  no  scars  or  evidences  of  fracture  of  the 
skull,  no  paralysis  or  other  indication  of  disturbance  of  the 
motor  tract. 

Usually,  however,  in  the  cases  which  give  no  sign  of 
direct  organic  injury,  the  latent  period  passes  without 
symptoms. 

Symptoms. — The  most  common  history  of  traumatic  epi- 
lepsy is  somewhat  as  follows  : 

A  man,  previously  healthy,  is  struck  on  the  head  by  a 
heavy  instrument,  or  falls  so  that  his  head  receives  a  severe 
blow,  which  inflicts  a  scalp  wound.  He  becomes  uncon- 
scious and  may  suffer  for  some  time  from  the  symptoms  of 
cerebral  concussion,  or  from  those  of  compression.  He 
eventually  recovers,  and  finds  that  one  side  of  the  body 
is  paralyzed.  The  paralysis  usually  rapidly  improves,  so 
that  when  the  patient  is  finally  examined  for  it  nothing 
remains  except  a  comparative  one-sided  weakness  or  stiff- 
ness or  a  unilateral  increase  of  the  deep  refiexes.  Some 
weeks  or  months  after  recovery  from  the  effects  of  the 
accident  the  patient  begins  to  have  convulsions  in  some 
portion  of  the  body  opposite  to  that  of  the  head  injury. 
The  twitchings,  which  are  usually  preceded  by  a  feeling  of 
numbness  or  tingling  in  the  affected  part,  begin  in  a  few 
muscles  and  then  spread  to  others.  They  are  expressive  of 
irritation  of  a  localized  portion  of  the  brain  cortex  and  are 
called,  after  their  original  describer,  Jacksonian.  In  the 
early  stages  of  the  disease  the  fits  often  remain  local,  but 
they  have  a  tendency  to  progress  so  that  they  eventually 
involve  the  whole  body,  although  usually  the  attack  con- 
tinues to  begin  in  the  part  first  affected.  Consciousness  is 
not  lost  in  the  earlier  attacks.     The  tendency  of  such  a  case, 


132  ORGANIC   EFFECTS   OF   INJURY.    ' 

however,  is  in  all  respects  progressive,  so  that  after  the  dis- 
ease has  existed  for  a  number  of  months  or  years  the  attacks 
become  exactly  similar  to  the  grmid  vial  of  idiopathic  epi- 
lepsy, with  the  possible  exception  that  they  may  continue 
to  begin  as  a  localized  spasm. 

On  examination  of  the  head  there  may  be  found  the  scar 
of  the  original  scalp  wound  and  a  depression  in  the  skull. 
The  scar  is  usually  not  tender,  and  pressure  upon  it  does 
not  cause  a  fit.  The  skull  may  be  fractured,  however,  even 
on  its  convexity,  without  leaving  any  sinking  in  of  its  sur- 
face. When  a  depression  exists,  the  injured  portion  of  the 
brain  is  not  necessarily  immediately  beneath  it.  The  bone 
may  be  splintered,  or  haemorrhage  may  have  occurred  in 
such  a  way  that  the  cerebral  lesion  is  situated  at  some  dis- 
tance from  the  site  of  the  external  injury.  The  frequency 
of  this  occurrence  is  fully  recognized  by  surgeons  who,  in 
operating  for  traumatic  epilepsy,  open  the  skull  at  a  point 
opposite  the  portion  of  the  cortex  which  supplies  the  mus- 
cles that  first  become  the  seat  of  spasm,  instead  of  being 
guided  by  the  depression  in  the  bone.  They  follow  the 
medical  rather  than  the  surgical  indications. 

The  typical  symptoms  of  traumatic  epilepsy  are  subject 
to  variations.  The  fits  may  take  other  forms  than  those  of 
muscular  spasm.  Petit  mal  is  a  common  and  sometimes  the 
sole  symptom.  Attacks  of  headache  may  be  substituted  for 
convulsive  phenomena,  as  is  shown  by  the  after-history  of 
Case  VI  of  Starr's  (Brain  Surgery) : 

J.  R.,  aged  forty,  was  struck  upon  the  left  temple  and  sus- 
tained a  fracture  of  the  skull  in  August,  1889.  When  he  recov- 
ered consciousness  he  was  found  to  be  paralyzed  upon  the  right 
side  and  aphasic.  In  the  course  of  the  following  six  months  the 
hemiplegia  slowly  subsided  and  the  speech  gradually  improved, 
so  that  he  was  able  to  go  about,  but  was  still  unfit  for  work. 
About  a  year  after  the  accident  he  began  to  have  convulsions ; 
some  of  these  were  general,  with  loss  of  consciousness,  but  later 
they  became  localized  and  remained   so  for  some   time.      They 


EPILEPSY. 


133 


increased  in  frequency  until,  when  seen  in  December,  1892,  the 
patient  was  having  several  every  week.  The  attacks  began  with 
a  twitching  of  the  muscles  about  the  mouth  upon  the  right  side; 
a  drawing  of  all  these  muscles  toward  the  right,  with  twitching 
of  the  eyes,  and  a  gradual  extension  of  the  spasm  to  the  right  side 
of  the  neck  and  to  the  right  arm  and  hand.  During  the  attack 
he  did  not  lose  consciousness,  but  he  could  not  speak,  and  ex- 
perienced a  sensation  of  tingling  in  the  face  and  mouth.  After 
an  attack  he  appeared  to  be  weak  and  was  not  able  to  talk  as  well 
as  before.  Examination  on  December  10,  1892,  demonstrated  a 
slight  paresis  on  the  right  side  of  the  face,  the  tongue  not  deviat- 
ing, and  some  weakness  in  the  right  arm,  but  no  affection  of  the 
leg;  no  disturbance  of  sensation;  increased  reflexes  upon  the 
right  side.  A  depressed  fracture  of  the  skull,  running  backward 
two  inches  about  over  the  position  of  the  Sylvian  fissure,  was 
evident  upon  palpation.  The  posterior  limit  of  the  fracture  was 
an  inch  below  the  location  of  the  motor  area  of  the  face.  At  the 
operation  a  considerable  amount  of  injury  to  the  meninges  and 
to  the  brain  substance  was  found  on  the  left  motor  region.  The 
patient  was  trephined  four  times. 

A  note  made  by  me  on  January  22,  1897,  four  years  later,  in 
the  Vanderbilt  clinic  records,  says  that  "  since  the  last  operation 
there  have  been  no  convulsive  seizures,  but  six  or  seven  times  a 
year  the  patient  has  attacks  of  headache  which  last  from  five  to 
six  hours.  The  pain  is  intense  and  consciousness  is  sometimes 
lost  temporarily.  During  one  of  these  attacks  the  patient  at- 
tempted suicide  on  account  of  the  pain. 

Traumatic  epilepsy  usually  becomes  in  time  an  exact 
clinical  counterpart  of  the  idiopathic  variety,  and  so  we  may 
expect  to  find  in  it  the  various  psychical  equivalents  which 
are  occasionally  encountered  when  the  disease  arises  from 
unknown  causes.  Still,  while  somnambulistic  attacks,  im- 
pulsive acts,  temporary  amnesias,  and  similar  phenomena 
may  occur,  they  do  not  constitute  a  prominent  feature  of 
the  traumatic  varietv  of  the  disease.  Many  of  the  morbid 
impulsions  of  cerebral  neurasthenia  and  some  of  the  symp- 
toms of  traumatic  insanity  are  epileptic  in  character,  being 
transitory  and  coming-  on  without  definite  warning ;  but 
unless  they  have   been  or   are  associated   with  convulsive 


134  ORGANIC   EFFECTS   OF    INJURY. 

seizures,  we  are  not  justified  by  our  present  knowledge  in 
calling  them  manifestations  of  epilepsy. 

The  course  of  traumatic  epilepsy  is  progressive.  The 
tendency  is  for  the  fits  to  become  uninterruptedly  more 
frequent  and  severe  and  to  be  coupled  with  a  constantly 
increasing  failure  of  mental  power.  In  some  cases  the  dis- 
ease appears  to  remain  stationary,  and  verv  rarely  the  fits 
are  said  to  have  ceased  altogether,  either  spontaneously  or 
through  the  influence  of  drugs.  However,  until  very  re- 
cent years,  recovery  was  practically  hopeless.  With  the 
advances  which  have  been  made  in  cerebral  surgery  the 
prognosis  has  become  somewhat  more  favorable.  Opera- 
tions have  in  certain  cases  been  the  means  of  ver}'  materi- 
ally lessening  the  number  and  severity  of  the  attacks,  and 
a  few  patients  appear  to  have  been  permanently  cured  by 
the  removal  of  sources  of  cortical  irritation.  But  the  re- 
sults of  trephining  for  epilepsy,  although  tangible,  have  not 
been  sufficiently  brilliant  to  warrant  the  disease  being  re- 
garded as  anything  but  a  very  serious  affection,  which, 
in  by  far  the  larger  number  of  cases,  is  incurable.  The 
chances  for  successful  treatment  are  greatest  when  the 
operation  is  done  immediately  after  the  accident ;  then,  by 
the  immediate  removal  of  splinters  of  bone  or  blood  clots,, 
the  brain  will  be  irritated  for  as  short  a  time  as  possible. 
In  any  case  in  which  the  fits  have  once  appeared  and  ex- 
isted for  any  length  of  time  the  hopes  for  recovery  are 
slight.  The  disease  in  itself  is  not  a  direct  menace  to  life, 
but  its  victims  are  in  constant  danger  of  accident.  They 
are  "risks"  which  life-insurance  companies  regularly  re- 
fuse to  accept. 

Diagnosis. — To  establish  beyond  reasonable  doubt  a 
causal  relationship  in  any  case  between  an  injury  and  the 
development  of  epilepsy  may  be  very  easy,  or  it  may  be 
practically  impossible.  In  persons  pre\nously  healthy  in 
whom  the  skull  is  shown  to  have  been  fractured,  there  will 


EPILEPSY.  J-- 

1-arely  be  any  question  as  to  the  relationship  between  the 
traumatisni  and  the  subsequent  convulsions.  But  if  exter- 
nal evidences  of  fracture  are  not  demonstrable,  there  are 
several  considerations  which  must  be  taken  into  account  be- 
fore it  can  be  stated  that  the  epilepsy  is  in  all  probability 
traumatic: 

I.  In  the  first  place  it  must  be  shown  that  the  patient 
had  never  had  general  convulsions  before  the  injury,  except 
such  convulsions  as  may  occur  in  infancy  without  beino- 
considered  as  expressions  of  idiopathic  epilepsy.  General 
convulsions  are  so  common  in  infancy  that  it  would  be 
manifestly  unjust  to  regard  as  epileptic  persons  who  had 
had  fits  in  the  first  year  or  two  years  of  life,  but  who  had 
subsequently  been  free  from  them. 

2.  The  general  condition  of  the  patient,  as  regards  alco- 
holism or  other  degenerative  evidences,  immediately  before 
the  accident,  must  be  considered,  especially  if  the  injury  is 
supposed  to  have  been  slight. 

3.  The  injury  itself  is  naturally  the  most  important  causal 
element.  If  it  results  in  hemiplegia  or  monoplegia,  the 
causal  connection  is  plain  ;  or  if  the  seizures  are  local,  and 
so  indicative  of  localized  brain  lesion,  there  will  rarely  be 
any  question  as  to  their  traumatic  origin.  Localized  muscu- 
lar spasm  as  a  symptom  of  idiopathic  epilepsy,  although  it 
has  been  observed,  is  extremely  rare,  and  it  would  probably 
never  occur  in  a  way  for  it  to  be  mistaken  for  the  local 
spasm  of  traumatic  epilepsy.  When  the  seizures  are  general, 
whether  they  depend  upon  injury  or  not  must  be  decided 
by  those  other  considerations  which  have  already  been 
mentioned. 

4.  The  time  elapsing  between  the  receipt  of  injury  and 
the  first  epileptic  manifestations  can  not  be  considered  as  a 
definite  guide  in  diagnosis.  The  statistics  are  derived  from 
those  cases  which  have  been  operated  upon,  and  in  most  of 
them  the  paroxysmal  symptoms  have  been  delayed  for  a 


1^6  ORGANIC  EFFECTS  OF  INJURY. 

few  weeks  or  a  few  months  after  the  accident.  Some  few 
cases,  which  in  other  respects  are  satisfactory  as  illustrative 
of  traumatic  epilepsy,  have  had  no  fits  until  several  years 
after  the  receipt  of  the  injury.  The  most  that  can  be  said 
in  this  respect  is  that  the  larger  number  of  cases  have 
developed  within  a  year  after  the  accident,  and  that  most 
of  the  cases  which  appear  after  longer  periods  of  time  are 
in  other  respects  less  typical  of  the  traumatic  form  of  the 
disease. 

5.  In  doubtful  cases  the  age  of  the  patient  may  be  of 
assistance  in  diagnosis.  Idiopathic  epilepsy  is  essentially  a 
disease  which  begins  in  childhood  and  adolescence.  Sixty 
per  cent  of  the  cases  occur  before  twenty  years  of  age,  and 
only  thirteen  per  cent  after  thirty.  Traumatic  epilepsy,  on 
the  other  hand,  is  almost  always  one  of  the  penalties  of  the 
exposure  to  accident  which  is  incident  to  the  active  periods 
of  life.  Of  course,  children  may  receive  severe  head  inju- 
ries, and  grown  men  sometimes  develop  idiopathic  epilepsy. 
But  the  two  diseases  belong  so  essentially  to  different  peri- 
ods of  life  that  traumatic  epilepsy  in  the  child  can  with  jus- 
tice be  diagnosticated  only  after  elimination  of  all  other 
causes  and  a  scrutinizing  study  of  attendant  circumstances. 
Conversely,  the  probability  is  greater  that  the  convulsions 
that  appear  after  injury  to  an  adult  who  has  never  had  fits, 
arise  as  the  direct  consequence  of  cerebral  injury. 

It  may  be  said,  in  conclusion,  that  no  case  of  epilepsy  in 
which  there  is  any  question  of  operation  or  of  medico-legal 
inquiry,  should  be  accepted  as  traumatic  without  the  seizures 
having  been  witnessed  by  a  physician  or  by  some  person 
trained  in  the  observation  of  the  symptoms  of  disease.  Such 
observation  can  best  be  carried  out  in  hospitals. 

Bibliography. 

Gray,  Epilepsy.  Dercums  Text -book  of  Nervous  Diseases  by 
American  Authors,  Philadelphia,  1895. 


GENERAL   PARALYSIS   OF   THE    INSANE. 


137 


Lloyd  and  Deaver,  A  Case  of  Focal  Epilepsy  Successfully 
Treated,  etc.     Am.  Jour,  of  the  Med.  Set.,  November,  1888. 

Starr,  Brain  Surgery,  New  York,  1893. 

Starr,  Familiar  Forms  of  Nervous  Disease,  New  York,  1890. 

Van  Gieson,  A  Contribution  to  the  Pathology  of  Traumatic 
Epilepsy.     JVew  York  AT edical  Record,  1893. 


General  Paralysis  of  the   Insane — General   Paresis 
— Dementia  Paralytica. 

An  inquiry  which  has  for  its  object  the  determination  of 
the  influence  of  trauma  upon  the  development  of  general 
paralysis  of  the  insane  is  beset  with  many  of  the  difficulties 
which  are  met  with  in  investigations  relative  to  the  trau- 
matic origin  of  tabes.  General  paresis,  like  tabes,  has  an 
initial  stage,  that  may  last  for  months  or  years,  during 
which  the  patient  is  not  only  not  incapacitated  for  work,  but 
may  conduct  himself  so  rationally  that  no  suspicion  is  enter- 
tained that  he  is  already  suffering  from  a  disease  which  is 
soon  to  destroy  both  mind  and  body.  From  the  insidiousness 
of  its  onset,  it  is  usually  impossible  to  say  even  approximately 
when  the  morbid  process  began.  In  non-traumatic  cases, 
when  the  first  marked  symptoms  consist  of  an  attack  of 
acute  maniacal  excitement  or  of  acute  mental  depression  or 
of  some  other  acute  manifestation,  there  is  every  reason  to 
suppose  that  the  disease  had  already  existed,  though  unsus- 
pected, for  some  time.  Similarly,  when  an  injury  to  the 
head  is  quickly  followed  by  an  outbreak  of  the  symptoms  of 
the  disease,  it  is  never  possible  to  say  with  absolute  certainty 
that  the  traumatism  did  anything  more  than  hasten  into  ac- 
tivity a  process  which  was  already  existent,  and  whose  ulti- 
mate development  was  inevitable,  irrespective. of  traumatic 
agency. 

Prodromal  Stage. — Inasmuch  as  it  is  so  often  the  sub- 
ject of  medico-legal  inquiry,  the  prodromal  stage  was  called 
by  Le  Grande  du  SauUe  "the  medico-legal  period."     How 


138  ORGANIC    EFFECTS   OF    INJURY. 

easily  it  may  pass  unsuspected  by  the  general  public  or  by 
medical  men  who  are  not  especially  versed  in  mental  dis- 
eases is  shown  by  an  incident  related  by  Le  Grande  du 
Saulle,  and  quoted  by  Hamilton : 

Two  brothers  went  to  the  office  of  a  Parisian  alienist,  and  the 
elder  had  a  private  consultation,  the  result  being  that  he  was  in- 
formed that  the  other  had  the  incipient  signs  of  paretic  dementia, 
and  that  death  would  occur  in  three  or  four  years.  They  de- 
parted, and  the  result  was  that  a  poUcy  of  insurance  was  procured 
for  one  hundred  thousand  francs.  Three  years  later  the  elder 
brother  pocketed  the  results  of  the  robbery. 

The  prodromal  symptoms  of  general  paresis  are  both 
physical  and  mental.  At  first  the  physical  symptoms  may 
be  nothing  more  than  a  slight  tremor  of  the  face  and  tongue 
with  some  indistinctness  of  speech.  Very  commonly  there 
is  an  early  myosis,  or  a  pupillary  inequality,  or  the  pupils 
may  show  the  Argyll-Robertson  phenomenon.  The  knee- 
jerks  are  lost  in  about  one  third  of  the  cases ;  in  the  others 
they  may  be  normal  or  may,  in  common  with  other  tendon 
reflexes,  be  exaggerated.  The  earliest  variations  from  the 
normal  mental  state  are  a  slight  forgetfulness,  inattentiveness, 
carelessness,  or  irascibility.  The  patient's  character  changes 
without  his  noticing  it.  "  Der  Kranke  wird  ein  Anderer,  und 
er  merkt  es  nicht."  The  delusions  of  grandeur  and  extrava- 
gant acts,  so  common  in  the  more  advanced  stages,  are  only 
occasionally  prominent  in  the  beginning  of  the  disease.'' 

These  mental  signs,  although  they  may  not  pass  unnoticed 
by  the  associates  or  by  the  family  of  the  patient,  rarely  ex- 
cite any  particular  remark  until  they  have  existed  for  some 
time,  and  have  become  disagreeably  prominent.  Then  in- 
quiry fails  to  fix  within  weeks  or  even  months  just  when  the 
changes  in  personality  began. 

To  determine  the  exact  part  played  by  any  exciting  cause 
in  a  disease  whose  beginning  is  practicably  never  determi- 
nable appears  well-nigh  impossible.     By  the  time  the  symp- 


GENERAL    PARALYSIS   OF    THE    INSANE. 


139 


toms  of  paresis  are  sufficiently  pronounced  for  the  patient 
to  be  brought  (he  rarely  comes  of  his  own  accord)  for  medi- 
cal examination,  the  disease  has  already  existed  for  some 
time ;  just  how  long  a  time  it  is  impossible  to  say,  but  cer- 
tainly long  enough  for  the  pa- 
tient's own  statements  to  have 
become  unreliable,  and  for  his 
friends  to  have  forgotten  when 
they  first  noticed  changes  in 
his  character.  Consequently, 
whether  any  alleged  cause  was 
so  far  responsible  for  the  dis- 
ease that,  had  the  cause  not 
existed,  the  disease  would  not 
have  developed,  will  be  a  mat- 
ter of  individual  opinion,  and 
must  be  largely  determined 
for  each  case.  The  most  that 
can  be  done  here  in  consider- 
ing the  influence  of  trauma  in 
the  causation  of  the  disease  is 
to  briefly  observe  the  general  setiology  and  to  review  the 
evidence  for  traumatic  agency. 

General  ^Etiology. — As  the  clinician  is  hampered  by  be- 
ing unable  to  recognize  the  disease  until  it  has  already  ex- 
isted for  a  considerable  length  of  time,  and  as  the  pathologist 
has  failed  to  reveal  the  fundamental  character  or  causation 
of  its  morbid  anatomy,  the  aetiology  of  general  paresis  re- 
mains imperfectly  understood. 

Among  the  general  ^etiological  factors  the  influence  of 
syphilis  is  the  most  easily  demonstrable.  There  is  a  varia- 
tion in  the  observations  of  different  investigators  as  to  the 
percentage  of  general  paralytics  in  whom  a  history  of  pre- 
ceding syphilis  is  obtainable,  but  all  agree  that  the  percent- 
age is  large. 


Fig.  32. — Showing;  characteristic  facial 
expression  in  the  early  stage  of  gen- 
eral paresis.     (Vanderbilt  Clinic.) 


140  ORGANIC   EFFECTS   OF   INJURY. 

In  Germany  it  is  given  by 

Mendell  and  Schnell.. . .  IK  per  cent  )  ^ 

-D-  u      u     i  Quoted  by 

Bmswanger 49-72  Y        Qebeke 

Ziehen 33-43    "       "      ) 

Gudden j  surely  357  per  cent; 

(  probably  9-6  per  cent. 

Hirschl  (Austria) 70  to  90  per  cent. 

56  per  cent  history  of  syphilis. 
25  per  cent  syphilis  probable. 
In  France  it  is  given  by 

Regis 70-90  per  cent. 

In  America  it  is  given  by 

Peterson 60-70  per  cent ; 

Bannister 89    "      " 

The  frequency  with  which  syphilis  has  preceded  general 
paresis  is  certainly  more  than  a  coincidence,  for  in  other 
forms  of  mental  disease  the  history  of  lues  is  not  obtainable 
in  over  15  to  20  per  cent.  In  what  way  the  syphilitic  poison 
causes  the  cerebral  degeneration  is  unknown.  Pathology 
has  failed  to  reveal  whether  it  acts  simply  as  a  predisponent, 
which  requires  the  addition  of  some  exciting  cause  to  induce 
the  disease,  or  whether  the  late  poisons  of  syphilis  are  of 
themselves  sufficient.  The  latter  alternative  seems  the  less 
probable  from  the  fact  that  while  syphilis  is  very  frequent, 
general  paresis,  compared  to  it,  is  rare.  If  syphilis  alone 
were  capable  of  producing  general  paresis,  it  would  be  rea- 
sonable to  suppose  that  the  relative  frequency  of  the  occur- 
rence of  the  two  diseases  would  be  more  equal.  Further- 
more,  general  paresis  is  different,  both  clinically  and  in  its 
pathological  anatomy,  from  the  affections  of  the  brain  char- 
acterized by  syphilitic  lesions.  However,  important  as  is 
the  relationship  between  syphilis  and  paresis,  it  is  not  abso- 
lute. There  are  cases  which  give  no  evidence  or  history 
of  syphilis,  and  in  which  the  pre-existence  of  syphilis  is  not 
even  probable.  Fournier,  who  believes  syphilis  to  be  the 
sole  cause  of  tabes,  admits  that  paresis  may  occur  without 
the  patient  having  had  the  venereal  disease. 


GENERAL    PARALYSIS   OF    THE    INSANE.  141 

There  are  other  predisposing  factors  which  must  be  con- 
sidered as  affecting-  causation.  Paresis  is  much  more  fre- 
quent in  males  than  in  females  (four  to  one,  Mickle).  In 
women  of  the  higher  classes  of  society  it  is  very  infrequent. 
The  disease  is  sharply  limited  by  age.  An  overwhelming 
majority  of  the  cases  occur  between  the  ages  of  thirty  and 
fifty ;  the  disease  is  very  rare  before  twenty-five,  and  rarely, 
if  ever,  occurs  after  sixty.  Heredity  may  often  be  found  to 
be  an  important  factor — not  in  the  sense  that  general  paresis 
is  directly  transmitted,  but  rather  that  the  individual  is  pro- 
vided with  a  brain  which  is  particularly  liable  to  succumb  to 
injurious  influences. 

The  causes  which  are  most  commonly  regarded  as  excit- 
ing in  the  aetiology  of  general  paresis  are  mental  excite- 
ment, worry,  and  overwork.  The  general  class  of  persons 
among  whom  the  disease  is  most  common,  the  greater  fre- 
quency with  which  it  occurs  in  the  inhabitants  of  cities,  and 
the  fact  that  it  appears  at  an  age  when  mental  and  bodily 
strain  are  at  their  highest  tension,  substantiate  the  hypoth- 
esis that  these  agencies  are  at  least  powerful  contributing 
causes. 

Trauma  as  a  Cause. — The  influence  of  accident  and 
injury  is  universally  regarded  as  important,  and  trauma 
appears  in  all  books  on  the  subject  as  one  of  the  principal 
exciting  agents.  General  injuries  are  sometimes  described 
as  determining  causes,  but  it  seems  extremely  improbable 
that  any  injury  can  be  regarded  as  sufficient  to  induce 
general  paresis  unless  the  blow  was  directly  applied  to  the 
head,  or  unless  there  was  a  considerable  shaking  up  of  the 
cranial  contents,  such  as  may  occur  in  concussion  acci- 
dents. In  only  a  few  of  the  reported  cases  has  the  skull 
been  fractured. 

The  percentage  of  traumatic  cases,  as  it  is  given  by  dif- 
ferent observers,  to  the  total  number  of  cases  of  general 
paresis  varies  greatly.     Schlager  says,  "  One  seventh  of  all 


J42  ORGANIC  EFFECTS  OF  INJURY. 

cases  of  mental  disease  induced  by  head  injuries  are  cases 
of  general  paralysis."  Meyer  found  fifteen  cases  of  injury 
to  the  head  in  seventy-six  cases  of  general  paresis,  in  which 
the  causes  "  were  clearly  made  out."  In  eighty  male  cases, 
Krafit-Ebing  found  cranial  injury  to  be  the  cause  in  six. 
Mickle  quotes  these  authors,  and  from  a  study  of  the  Eng- . 
lish  Lunacy  Reports  finds  six  per  cent  of  the  cases  in  both 
sexes  as  due  to  head  injuries. 

Christian  observed  forty-three  cases  of  general  paresis 
in  one  hundred  cases  of  injuries  to  the  skull.  In  five  hun- 
dred cases  of  insanity  Schlager  ascribed  a  traumatic  aetiol- 
ogy to  forty-nine,  of  which  seven  developed  general  paresis. 

Gudden  reports  forty-five  cases  in  which  a  history  of 
head  injury  was  prominent.  In  six  of  these  the  trauma  had 
occurred  in  childhood,  years  before  the  symptoms  of  the 
general  brain  disease.  In  eighteen  the  trauma  and  the  par- 
alytic symptoms  were  separated  by  a  period  varying  from 
six  months  to  twenty  years ;  and  in  twenty-one  the  para- 
lytic symptoms  developed  in  direct  sequence  (few  months) 
upon  the  head  injury.  The  accident  was  generally  accom- 
panied by  loss  of  consciousness,  and  in  four  cases  the  skull 
was  fractured.  Of  one  hundred  and  seventy-five  cases  re- 
ported by  Hirschl,  trauma  had  exerted  an  influence  in  7.4 
per  cent. 

From  the  above  reports  of  traumatic  general  paresis 
it  appears  that  the  injury  was  incurred  in  the  great  major- 
ity of  cases  by  falls*  or  by  blows  on  the  head  received  in 
brawls.  Now,  the  disease  is  characterized  by  momentary 
attacks  of  dizziness  or  unconsciousness,  which  may  cause 
the  patient  to  fall  and  strike  his  head,  by  an  inattention 
which  exposes  him  to  a  variety  of  accidents,  and  especially 
by  an  excitable  mental  state,  which  frequently  leads  him  into 
those  animated  discussions,  as  a  result  of  which,  somebody's 
head  is  often  injured.  And,  indeed,  it  seems  as  though  the 
receipt  of  head    injury   was  a  result  of   the   disease  rather 


GENERAL   PARALYSIS   OF    THE   INSANE, 


143 


than  the  cause  of  it  in  by  far  the  larger  number  of  the  pub- 
lished cases.  The  following  case  illustrates  a  history  of  the 
disease  such  as  is  usually  described  as  traumatic,  but  in 
which  the  patient  was  undoubtedly  suffering  from  paresis 
before  the  occurrence  of  the  accident : 

A.  G.,  forty  years  of  age,  came  to  the  Vanderbilt  clinic  on 
December  18,  1893.  Syphilis  and  alcoholism  denied.  The  pa- 
tient says  he  was  well  until  six  months  previously,  when  he  fell 
from  a  building.  He  did  not  lose  consciousness,  but  was  in  bed 
two  weeks  with  a  swollen  ankle.  No  paralysis.  Two  months 
later  right  hemiplegia  and  motor  aphasia  suddenly  developed, 
lasted  for  two  weeks,  and  then  as  suddenly  disappeared.  A  simi- 
lar attack  of  paralysis,  also  temporary,  occurred  a  short  time 
afterward,  and  was  followed  in  a  few  days  by  an  attack  of  motor 
aphasia,  unaccompanied  by  loss  of  muscular  power.  The  day  be- 
fore I  saw  the  man  he  had  had  convulsions  in  both  arms  without 
any  loss  of  consciousness.  Examination  showed  no  paralysis, 
no  ataxia,  pupils  equal  and  reacting  to  light,  knee-jerks  absent. 
Temporal  limitation  of  the  visual  fields;  tremor  of  face,  tongue, 
and  hands  very  marked  ;  speech  and  expression  characteristic  of 
general  paresis. 

There  was  no  question  as  to  the  diagnosis  of  the  disease  from 
which  the  patient  was  suffering,  but  the  apoplectiform  character 
of  its  course  indicated  very  conclusively  that  the  fall  had  not,  as 
the  patient  claimed,  caused  the  disease,  but  had  been  a  result  of 
one  of  the  earliest  seizures. 

How  necessary  it  is  to  consider  every  factor  before 
ascribing  to  trauma  a  place  in  the  causation  of  general  pa- 
resis is  well  shown  by  the  following  case.  Inasmuch  as  it 
is  soon  to  become  the  subject  of  litigation,  there  will  be  no 
mention  of  names,  dates,  or  places  in  describing  it: 

A  man,  thirty-three  years  of  age,  consulted  a  physician  on 
account  of  an  injury  which  he  had  received  six  weeks  previously. 
The  patient  denied  having  had  syphilis,  and  said  that  he  had 
always  been  a  strong  and  healthy  man  until  an  accident  in  which 
he  was  struck  on  the  head  and  knocked  down  by  a  passing  vehi- 
cle. As  a  result  of  the  injury  he  was  carried  to  a  hospital,  and 
lay  there  unconscious  for  eight  days.  He  then  quickly  recovered 
and  returned  to  work,  although  still  troubled  with  the  headaches. 


144  ORGANIC    EFFECTS   OF   IN7URY. 

for  which  he  sought  medical  advice.  The  examination  showed 
tremor  of  the  face,  lips,  and  tongue,  thickness  of  speech,  inequal- 
ity in  the  size  of  the  pupils,  though  both  responded  readily  to 
light  and  during  efforts  at  accommodation.  All  the  tendon  re- 
flexes were  active,  but  there  was  no  paralysis.  The  general  ap- 
pearance and  manner  were  those  of  a  patient  with  general  paresis. 
The  gait  was  careless,  the  memory  poor,  the  attention  defective. 
The  diagnosis  and  the  evaluation  of  the  influence  of  the  injury 
were,  however,  postponed  until  further  information  could  be  ob- 
tained. 

From  the  house  surgeon  of  the  hospital  where  the  man  was 
taken  after  the  accident  it  was  learned  that  on  admission  the 
patient  was  delirious  and  was  paralyzed  in  one  arm,  but  had  no 
external  injuries  except  a  slight  abrasion  on  one  cheek.  The 
mental  condition  resembled  that  of  acute  mania,  with  great  excite- 
ment, delusions,  and  hallucinations.  These  soon  passed  away, 
however,  as  did  also  the  paralysis  of  the  arm. 

Witnesses  of  the  accident  said  that  the  man  fell  against  the 
vehicle,  instead  of  the  vehicle  running  into  him.  His  wife  admit- 
ted that  for  a  year  before  the  accident  her  husband  had  been  for- 
getful, irritable,  and  subject  to  headaches;  that  she  had  noticed 
that  one  pupil  was  larger  than  the  other;  that  there  had  occurred 
from  time  to  time  paralysis  of  one  arm  or  of  one  leg,  or  loss  of 
the  power  of  speech,  but  that  these  symptoms  would  pass  away 
completely  in  a  day  or  two.  She  also  admitted  that,  having 
been  pregnant  seven  times,  she  had  never  given  birth  to  a  living 
child,  the  abortion  always  occurring  in  the  sixth  or  seventh  month. 
These  facts,  together  with  subsequent  observations  of  the  patient, 
during  which  the  symptoms  became  more  marked,  left  little 
doubt  as  to  the  correctness  of  the  diagnosis  of  general  paresis; 
but  they  proved  conclusively  that  it  was  not  traumatic  general 
paresis.  The  patient  was  in  all  probability  syphilitic,  as  shown 
by  the  barrenness  of  his  wife,  who  is  a  strong,  healthy-looking 
woman  ;  the  mental  disease  had  begun  at  least  a  year  before  the 
accident,  as  shown  by  the  attacks  of  paralysis,  the  headaches,  the 
inequality  of  the  pupils,  etc. ;  the  accident  was  in  all  probability 
a  result  of  the  disease,  inasmuch  as  the  witnesses  said  that  the 
patient  fell  and  was  then  hit  by  the  vehicle.  Accordingly,  in  this 
case,  in  the  absence  of  external  evidences  of  injury,  it  is  reason- 
able to  maintain  that  the  accident  exerted  little  or  no  influence 
upon  the  course  of  the  disease.  It  would  probably  not  have  oc- 
curred to  a  healthy  man,  but  was  one  of  the  unavoidable  penal- 


GENERAL    PARALYSIS    OF    THE    INSANE.  145 

ties  which  are  paid  by  persons  who  are  unable  to   take  care  of 
themselves. 

Cases  similar  to  these  have  undoubtedly  been  the  cause 
of  much  misapprehension  as  to  the  part  played  by  injury  in 
the  causation  of  general  paresis.  The  patient  may  himself 
believe  in  the  truth  of  the  history  he  tells  regarding-  occur- 
rence of  the  traumatism,  but  the  mental  state  of  a  disease 
which  is  characterized  by  delusions,  hallucinations,  and  con- 
fusion render  untrustworthy  all  the  statements  which  may 
be  made  by  any  one  suffering  from  it. 

If  the  disease  is  sufficiently  advanced  to  be  diagnosti- 
cated, there  is  no  more  reason  for  the  physician  to  accept 


Fig.  22. — "  This  is  a  fine  day  for  the  first  of  June."     Handwriting  of  a  patient  in  the 
early  stage  of  general  paresis.     (Vanderbilt  Clinic.) 

the  patient's  statements  regarding  accident  or  injury  than 
there  is  to  believe  the  expressions  of  grandiose  ideas  or  of 
depression,  or  the  assertions  of  magnificent  health  in  a  per- 
son who  is  evidently  doomed.  Consequently,  no  case  of 
general  paresis  can  be  reasonably  regarded  as  of  traumatic 
origin  unless  the  testimony  of  credible  witnesses  shows  that 
the  injury  was  the  result  of  an  accident  which,  as  far  as  the 
victim  was  concerned,  was  unavoidable. 

When  it  can  be  shown  that  the  head  injury  was  in  no 
way  the  result  of  the  disease,  but  was  the  consequence  of 


1^6  ORGANIC   EFFECTS   OF   INJURY. 

one  of  the  many  accidents  to  which  all  people  are  com- 
monly  exposed,  it  is  necessary  to  determine  as  clearly  as 
possible  in  how  far  the  traumatism  was  responsible  for  the 
development  of  the  disease. 

The  inquiry  should  be  especially  painstaking  as  regards 
three  points  : 

1.  In  the  first  place,  to  avoid  gross  errors  in  diagnosis, 
it  must  be  proved  that  the  course  and  character  of  the 
symptoms  are  identical  or  closely  allied  with  those  of  gen- 
eral paresis.  After  many  head  injuries,  especially  if  the 
skull  has  been  fractured  or  there  has  been  intracranial 
haemorrhage  or  brain  laceration,  there  develops  a  condition 
of  delirium  and  excitement,  at  the  subsidence  of  which  the 
patient  passes  into  a  condition  of  more  or  less  complete 
dementia.  Associated  with  the  mental  symptoms  there 
may  be  the  dysarthria,  the  evidences  of  localized  paralyses, 
the  tremors,  and  other  signs  similar  to  those  which  occur 
in  general  paresis.  These  patients  may  die,  in  which  event 
the  lesions  found  are  more  localized  and  more  prominent 
than  those  of  general  paresis ;  or  they  may  improve  and 
live  in  good  physical  health,  although  demented,  for  many 
years.  Some  of  them  present  such  striking  similarities  to 
the  cases  of  general  paresis  that  it  is  only  by  the  obser- 
vation of  them  for  considerable  periods  of  time  that  it  can 
be  decided  that  the  underlying  anatomical  process  must  be 
essentially  different. 

2.  The  question  of  predisposition  is  very  important  in 
cases  alleged  to  have  resulted  from  trauma. 

In  nearly  all  the  reported  cases  of  general  paresis  which 
have  followed  injury,  in  which  the  receipt  of  the  injury 
of  itself  might  not  have  been  regarded  as  a  symptom  of 
the  disease,  there  was  evidence  that  a  strong  predisposi- 
tion, either  hereditary  or  acquired,  had  pre-existed.  ■  The 
hereditary  predisposition  has  been  proved  by  the  family 
history,  by  congenital  syphilis,  or  by  the  stigmata  of  degen- 


GENERAL    PARALYSIS   OF    THE    INSANE. 


147 


eralion.  The  acquired  predisposition  has  consisted  in  the 
results  of  preceding-  syphilis.  Of  all  these  factors  syphilis 
is  the  most  important.  In  view  of  the  fact  that  syphilitic 
processes  become  much  more  active  after  traumatisms,  in- 
jury is  often  regarded  as  of  minor  setiological  importance 
if  it  is  soon  followed  by  paretic  symptoms  in  an  individual 
who  is  undeniably  syphilitic,  although  he  may  never  have 
presented  any  cerebral  symptoms  before  the  accident. 
This  is  hardly  just.  To  deny  a  traumatic  origin  to  the 
disease  because  the  patient  has  had  syphilis,  appears  to 
me  to  be  equivalent  to  saying  that  the  patient  would  have 
had  paresis  whether  his  head  had  been  injured  or  not. 
Such  a  view  is  not  warranted  by  our  present  knowledge. 
Similarly  to  what  will  be  said  concerning  locomotor  ataxia, 
there  are  so  many  syphilitic  persons  who  receive  severe 
head  injuries  without  developing  general  paresis,  that  in 
any  syphilitic  person  in  whom  head  injury  is  quickly  fol- 
lowed by  the  symptoms  of  the  mental  disease  it  seems 
more  reasonable  to  ascribe  to  the  traumatism  an  influence 
at  least  equal  to  that  of  the  venereal  infection.  However, 
this  matter  will  always  be  one  of  individual  opinion.  Most 
of  the  cases  of  paresis  occurring  after  head  injury  have  had 
syphilis,  and  it  is  never  possible  to  decide  positively  as  to 
the  relative  value  of  the  two  factors.  The  number  of  re- 
corded cases  of  persons  who  were  syphilitic,  yet  who  pre- 
sented no  symptoms  of  brain  disease  until  after  the  receipt 
of  a  head  injury,  is  not  small.     Thus, 

Mickle  tells  of  the  case  of  a  soldier  with  a  long  syphilitic  his- 
tory who  suffered  a  severe  injury  to  the  head  in  July,  and  on  the 
29th  of  that  month  was  admitted  to  the  hospital  with  maniacal 
symptoms.  Seven  weeks  afterward  he  was  discharged  to  duty, 
but  was  readmitted,  in  the  January  following,  with  general  pare- 
sis, the  onset  of  which  had  been  characterized  by  the  mental  symp- 
toms which  followed  closely  upon  the  cranial  injury. 

In  similar  cases  the  syphilis  has  preceded  the  paresis  by 
a  period  varying  from   one  to  twenty  years,  and  the  first 


148  ORGANIC   EFFECTS   OF    INJURY. 

mental  symptom  had  appeared  in  a  few  months  or  years 
after  the  accident. 

3.  Can  a  person  who  has  never  had  syphilis,  or  marked 
hereditary  predisposition,  develop  general  paresis  as  the 
direct  consequence  of  injury  to  the  head  ? 

Dr.  L.  C.  Pettit,  of  the  Manhattan  State  Hospital,  Ward's 
Island,  New  York,  whose  extensive  researches  bearing  upon 
this  disease  are  well  known,  tells  me  that  "from  a  study  of 
two  thousand  clinical  histories  he  is  forced  to  believe  that 
traumatism  is  not  to  be  regarded  as  a  sole  cause  of  the  dis- 
ease. In  over  one  hundred  autopsies  made  on  paretics  he 
has  only  once  seen  anything  which  seemed  to  be  correlative 
to  traumatism.  In  one  case,  over  the  region  of  the  right 
gyrus  occipitalis  superior,  there  was  a  depression,  about  the 
size  of  a  silver  twenty-five-cent  piece,  of  the  inner  table  of 
the  skull,  which  was  the  result  of  injury.  In  exactly  the 
same  area  on  the  left  hemisphere  there  was  necrosis  of  the 
cerebral  cortex." 

In  reference  to  trauma  as  a  sole  cause,  Mickle  says :  "  In 
cases  which  have  come  under  my  own  observation,  where 
cranial  injury  has  conduced  to  general  paresis,  it  has,  in  the 
majority,  seemed  to  play  the  part  of  a  predisposing  rather 
than  of  an  exciting  cause.  In  speaking  of  cranial  injury  as 
a  predisposing  cause  of  general  paresis,  we  may  suppose 
that,  in  consequence  of  latent  residual  results  of  the  imme- 
diate effects  of  trauma,  either  the  cerebral  tissues  are  simply 
less  resistant  to  the  influences  of  the  ordinary  causes  of  the 
pathological  process  which  underlies  general  paresis,  or  that 
this  process  springs  more  fully  into  being  by  assisting  in, 
and  in  its  turn  being  assisted  by,  the  intensification  and  ex- 
tension of  slight  local  inflammation  or  hyperplasia  sequen- 
tial to  the  brain  injury ;  or,  again,  assisted  by  morbid  vaso- 
motor effects  of  that  injury." 

The  views  of  these  observers  seem  to  be  substantiated 
by  clinical  experience.     I   have  been  unable  to  find  in  all 


GENERAL   PARALYSIS   OF   THE    INSANE.  149 

literature  a  single  case  of  traumatic  general  paresis  in  which 
sufficient  details  were  given  to  justify  the  absolute  conclu- 
sion that  the  head  injury  was  the  one  cause  of  the  disease. 

The  number  of  cases  in  which  there  is  even  a  possibility 
of  traumatism  being  the  exclusive  cause  is  very  small.  The 
most  complete  one  is  reported  by  Fox ;  but  that  observer 
himself  admitted  that  the  disease  might  have  existed  pre- 
viously to  the  receipt  of  the  injury  : 

"The  patient  was  a  man,  forty-nine  years  old,  married  eighteen 
and  a  half  years;  eleven  children;  wife  miscarried  once  with  twins. 
Family  and  personal  history  clear.  No  syphilis.  Formerly  a  cool, 
collected,  precise,  sober,  and  particularly  neat  man,  who  had  al- 
ways enjoyed  very  good  bodily  health.  On  December  27th  was 
thrown  out  of  a  trap,  striking  on  h'is  head.  His  wife  asserts  that  he 
was  in  perfect  mental  health  up  to  the  time  of  the  accident,  and  that 
some  unusual  irritability  which  had  been  noticed  was  simply  due  to 
a  heavy  cold,  which  his  previous  excellent  mental  health  had  un- 
fitted him  to  bear  patiently.  Whether  this  was  or  was  not  the  case, 
it  is  certain  that,  a  day  or  two  after  the  accident,  various  symptoms 
suggestive  of  general  paresis  appeared;  so  that,  if  the  disease  had 
not  an  exclusively  traumatic  origin,  its  development  and  first  mani- 
festation at  least  were  determined  by  accident.  The  first  day  after 
the  fall  he  complained  of  pain  in  his  head,  but  after  the  first  day 
made  no  complaints,  but  said  he  was  never  better  in  his  life." 

Sixteen  days  after  the  accident,  when  admitted  to  the  hospital, 
the  physical  and  mental  symptoms  of  general  paresis  were  easily 
recognizable.    The  disease  pursued  a  characteristic  and  fatal  course. 

Another  case  is  reported  by  Van  Deventer  (quoted  by 
Bechholm : 

A  stonecutter,  thirty  years  old,  father  alcoholic,  patient  himself 
slightly  alcoholic,  but  no  history  of  syphilis.  He  was  struck  in  the 
left  temple  by  a  piece  of  marble  and  lost  consciousness  momenta- 
rily, but  continued  with  his  work  after  a  few  moments.  The  next 
day  he  became  aphasic  for  twenty-four  hours,  restless,  and  un- 
willing to  stay  in  bed.  Had  headache  and  insomnia.  A  few  days 
later,  had  an  attack  of  violence  and  confused  ideas  of  persecution. 
He  entered  the  asylum  three  weeks  after  the  accident,  present- 
ing symptoms  of  amnesia,  megalomania,  with  hallucinations  and 
persecutory  ideas.  Seven  months  later  occurred  clonic  spasms 
II 


I50  ORGANIC   EFFECTS   OF   INJURY. 

and  apoplectiform  attacks;  seventeen  months  later,  difficulties  of 
speech,  tremor,  inequality  of  the  pupils,  and  weakness  of  all  the 
muscles.  The  patient  died,  twenty-five  months  after  the  accident^ 
with  symptoms  of  complete  dementia. 

Neither  of  these  cases  is  conclusive  evidence  for  the 
existence  of  traumatism  as  a  sole  cause  of  general  paresis, 
but  they  are  the  best  evidence  we  have. 

In  default  of  better  proof  of  the  traumatic  origin  of  a 
disease  which  is  so  common  and  which  has  so  frequently 
been  the  subject  of  medico-legal  inquiry,  the  conclusion  is 
unavoidable  that  if  trauma  is  ever  the  sole  cause  of  general 
paresis,  such  a  causal  relationship  is  extremely  unusual  and 
difficult  of  proof,  and  is  only  to  be  accepted  after  scrupu- 
lous inquiries  have  eliminated  all  of  the  many  opportunities 

of  error. 

Bibliography. 

Bechholm,  Maladies  mentales  d'origine  traumatique.  These 
de  Paris,  1896. 

Bannister,  Am.  Jour,  of  Itisanity,  i893-'94,  p.  477. 

Christian,  Des  traumatismes  du  crane  dans  leurs  rapports  avec 
I'alienation  mentale.     Arch,  de  neuroL,  Juillet  et  Sept.,  1889. 

Fournier,  Gaz.  nie'd.  de  Paris,  November  3,  1894. 

Fox,  Unusual  Cases  of  General  Paresis.  Jour.  Ment.  Science, 
1891,  p.  393. 

Gudden,  Zur  Aetiologie  u.  Sympt.  der  prog.  Paralysie  mit  be- 
sonden  Beriick.  des  Trauma,  etc.     Arch.  f.  Psych.,  February,  1894. 

Hamilton,  System  of  Legal  Medicine,  New  York,  1894. 

Hirschl,  Die  Aetiologie  der  prog.  Paralyse.  Abs.  Neurol.  Cblatt.y 
1896,  p.  369. 

Jacobson,  Traumatische  Psychosen.  Nord.  Med.  Ark.,  1893, 
iii,  13,  p.  I. 

Mickle,  General  Paralysis  of  the  Insane,  London,  1886. 

Ibid.,  General  Paralysis  from  Cranial  Injury.  Jour.  Ment.  Sci.^ 
January,  1883,  p.  545. 

Oebeke,  Zur  Aetiologie  der  allgemeinen  fortsch.  Paralyse. 
Zeit.  fiir  Psych.,  1891,  xlix,  p.  i. 

Peterson,  Relation  of  Syphilis  to  General  Paresis.  New  York 
Med.  Pec,  December  9,  1893. 

Regis,  Manual  of  Mental  Med.,  Syracuse,  1894.     (Trans.) 

Schlager,  quoted  by  Hudden.     Op  cit. 


LOCOMOTOR   ATAXIA.  jci 


Locomotor  Ataxia — Tabes  Dorsalis. 

Although  locomotor  ataxia  is  one  of  the  commonest  of 
the  chronic  degenerative  diseases  of  the  nervous  system, 
there  is  very  little  definite  knowledge  regarding  its  patho- 
genesis, and  many  difficulties  stand  in  the  way  of  a  complete 
understanding  of  its  nature.  The  disease  is  not  in  itself 
a  direct  menace  to  life,  and  in  the  cases  which  come  to  au- 
topsy the  morbid  process  has  existed  for  so  long  a  time  and 
has  become  so  advanced  and  so  extensive  that  it  is  impossi- 
ble to  tell  when  it  had  its  beginning.  Until  we  know  which 
nervous  element  is  first  affected,  we  can  not  hope  to  know 
very  much  about  the  etiology  of  the  disease.  Another  diffi- 
culty in  the  study  of  its  pathology  is,  that  although  only  cer- 
tain portions  of  the  cerebro-spinal  axis  are  involved,  there  is 
nothing  about  the  microscopic  appearances  of  the  lesion 
itself  which  are  exclusively  characteristic.  Its  funda- 
mental anatomical  character  is  a  degeneration  of  the  pos- 
terior columns  in  the  spinal  cord,  with  which  are  usually 
associated  an  inflammation  of  the  pia  mater  and  a  degenera- 
tion of  the  posterior  nerve  roots  and  of  the  spinal  ganglia. 
It  is  essentially  a  degeneration  of  nerve  fibers  and  nerve 
cells,  associated  with  a  growth  of  connective  tissue  and 
sometimes  with  degeneration  of  the  walls  of  the  blood- 
vessels. All  these  morbid  changes  are  found  in  other  dis- 
eases. Even  the  clinical  fact  that  syphilis  frequently  pre- 
cedes tabes  receives  no  substantiation  from  the  microscopical 
anatomy  of  the  latter  disease.  From  a  study  of  the  spinal 
cord  alone  in  a  case  of  tabes  it  would  be  impossible  to  say 
whether  the  patient  had  or  had  not  had  syphilis.  Whatever 
the  pathological  nature  of  tabes  may  be,  it  is  certainly  some- 
thing more  than  spinal  syphilis.  It  is  conjectured  that  the 
ultimate  products  of  the  syphilitic  virus  exercise  a  select- 
ive action  on  certain  portions  of  the  spinal  cord  or  of  its 
nerve  roots,  and  that  the  tabetic  degeneration  is  in  reality 


152  ORGANIC   EFFECTS   OF    INJURY. 

syphilitic.  Although  this  view  may  be  correct,  it  is  largely 
speculative  and  lacks  anatomical  proof.  In  the  absence  of 
such  proof  it  is  unjustifiable  to  claim  an  absolute  causative 
influence  for  syphilis. 

But  though  the  morbid  anatomy  of  tabes  has  been  of 
little  or  no  service  in  determining  the  causation  of  the  dis- 
ease, it  has  yielded  an  important  result  in  showing  that  the 
character  of  the  lesion  is  degenerative  rather  than  actively 
inflammatory,  and  that  it  requires  a  considerable  time  for  its 
development.  The  nerve-fiber  degeneration,  the  connective- 
tissue  growth,  the  vascular  abnormities,  all  bespeak  a  pro- 
cess which  is  essentially  slow,  and  argue  against  the  possi- 
bility of  the  disease  reaching  a  marked  degree  of  develop- 
ment within  a  few  days  or  weeks. 

Pre-ataxic  Period. 

The  clinical  difficulties  which  are  met  with  in  attempts 
to  elucidate  the  mysteries  surrounding  this  disease  arise  from 
the  insidiousness  of  its  onset,  the  extreme  chronicity  of  its 
course,  and  the  uncertain  character  of  its  causes.  Locomotor 
ataxia  is  the  most  chronic  of  all  degenerative  nervous  dis- 
eases. It  may  exist  without  seriously  impairing  the  general 
health  of  the  patient  for  ten,  twenty,  thirty,  or  even  a  greater 
number  of  years  after  its  existence  has  become  recognized. 
How  long  it  may  last  before  any  symptoms  become  appar- 
ent is  not  definitely  known,  but  certainly  for  a  considerable 
length  of  time.  A  patient  of  mine,  fifty-two  years  of  age,  who 
had  syphilis  thirty  years  ago,  has  been  in  the  pre-ataxic  state 
for  five  years.  Both  knee-jerks  are  absent,  there  is  loss  of 
sexual  power,  the  right  pupil  is  larger  than  the  left  and  pre- 
sents the  Argyll-Robertson  phenomenon,  and  there  is  a  dimi- 
nution of  sensibility  in  the  ulnar  distribution  of  both  hands. 
These  signs  are  sufficient  for  a  diagnosis  of  tabes,  al- 
though, aside  from  a  slight  swaying  of  the  body  on  standing 
with  closed  eyes,  there   are  absolutely   no  disturbances   of 


LOCOMOTOR   ATAXIA. 


153 


motion,  and  there  have  never  been  characteristic  pains.  The 
patient  came  to  me  originally  for  alcoholism,  and  the  tabetic 
symptoms  were  discovered  during  the  course  of  a  routine 
examination. 

The  pain  is  usually  the  cause  of  the  patient  seeking  med- 
ical advice,  although  there  are  other  frequent  initial  symp- 
toms observed  by  the  patient,  such  as  slight  ataxia,  difficulty 
in  urination,  and  disturbances  of  vision. 

The  condition  of  the  bones  and  joints,  which  predisposes 
them  to  disease  or  fracture,  is  sometimes  the  means  of  first 
calling  attention  to  the  existence  of  the  spinal  degeneration. 

Some  time  ago  a  patient  came  to  the  Vanderbilt  clinic  with 
extreme  enlargement  of  the  right  knee  joint,  which  he  said  was 
the  result  of  a  fall  received  a  month  previously.  Although  he 
did  not  know  it,  the  man  presented  classical  symptoms  of  tabes, 


Fig.  34. — Charcot  joint,  the  alleged  result  of  traumatism.     (Incurable  Hospital.) 


which  must  have  existed  long  before  the  accident  ;  and  although 
the  particular  lesion,  which  has  proved  to  be  a  Charcot  joint,  may 
have  been  to  a  certain  extent  influenced  by  the  injury,  it  occurred 
in  an  individual  predisposed  by  tabes  to  its  development. 

The  photograph  in  Fig.  34  is  of  a  Charcot  joint  in  a  patient 
who  presents  nearly  all  the  symptoms  of  advanced  tabes.  He 
says  he  was  perfectly  well  until  he  fell  on  the  right  knee,  as  a 
result  of  which  it  became  enlarged,  a  condition  which  was  followed 
by  other  characteristic  symptoms.    As  the  accident  occurred  years 


154 


ORGANIC  EFFECTS  OF  INJURY. 


before  the   patient  came   under   observation,   it   is  impossible  to 
prove  the  incorrectness  of  his  belief. 

Even  in  the  clinically  early  stages,  during  which  the 
patient  is  usually  conscious  of  one  symptom  only,  or  of  no 
symptoms  at  all,  a  careful  examination  will  show  that  there 
are  already  present  objective  evidences  of  structural  disease 

of  connecting  paths 
which  must  have 
been  present  for  a 
considerable  length 
of  time,  and  which 
must,  in  all  proba- 
bility, have  ante- 
dated any  subjec- 
tive discomfort.  In 
default  of  such  ob- 
jective evidences, 
the  diagnosis  of  ta- 
bes can  not  with 
certainty  be  made. 
The  most  common 
of  diagnostic  signs 
are  the  loss  of  one 
or  both  knee-jerks, 
the  Argyll-Robert- 
son pupil,  and  the 
Romberg  symptom. 
One  or  all  of  these 
three  symptoms — 
the  cardinal  symp- 
toms— are  very  con- 
stant, and  usually 
appear  early,  but 
none  of  them  would 

Fig.  35. — Attitude  of  static  ataxia. 

(Vanderbiit  Clinic.)  be    noticed    by    the 


LOCOMOTOR   ATAXIA. 


155 


patient,  and  would  ordinarily  be  overlooked  in  any  med- 
ical examination  in  which  a  determination  of  the  condition 
of  the  nervous  system  were  not  a  primary  object.  Similarl}'^ 
with  tactile  anaesthesia  of  the  trunk;  the  patient  is,  in  early 
stages,  unconscious  of  it  until  it  is  demonstrated  by  the  phy- 
sician. It  is  often  one  of  the  earliest  of  tabetic  manifesta- 
tions. 

Fig.  36  shows  the  tactile  ansesthesia  chart  of  a  patient  whose 
•only  other  symptoms  are  sUght  unsteadiness  of  gait  and  loss  of 
knee-jerk. 

That  the  early  symptoms  of  tabes  are  often  overlooked  is 
a  fact  of  common  experience,  for  it  occurs  not  infrequently 


Fig.  36. — Tactile  anaesthesia  in  a  patient  in  the  early  stage  of  locomotor  ataxia. 

that  persons  suffering  from  incipient  tabes,  when  the  only  sub- 
jective symptoms  are  pain  or  perhaps  slight  unsteadiness  of 
gait,  are  seen  by  physicians  who  are  unfamiliar  with  the 
diagnosis  of  nervous  diseases  and  who  treat  such  cases  with- 
out knowing  upon  what  fundamental  conditions  the  symp- 
toms depend.     No  examination  of  the  knee-jerks  or  of  the 


10  ORGANIC   EFFECTS   OF   INJURY. 

pupils  is  made,  and  the  condition  is  regarded  as  sciatica  or 
"  spinal  congestion."  There  can  be  no  doubt  that  in  many 
cases  the  cardinal  symptoms  exist  for  months  or  years  with- 
out the  patient's  knowledge,  and  the  physician  who  eventu- 
ally finds  any  one  of  them  finds,  not  a  recent  symptom,  but 
one  whose  character  has  permitted  it  to  exist  a  long  time 
unsuspected  ;  or  the  patient  may,  while  in  the  pre-ataxic 
stage,  have  consulted  a  physician  for  other  troubles,  but 
unless  at  that  time  he  complained  of  subjective  nervous 
symptoms  as  well,  there  would  probably  have  been  no  exam- 
ination of  the  pupillary  or  patellar  reflexes.  Without  such 
examination  it  would  be  impossible  to  assert  that  the  patient 
were  free  from  spinal  disease.  Similarly,  the  fact  that  the 
patient  had  been  a  successful  candidate  for  life  insurance 
would  not  be  an  absolute  guarantee  that  he  were  at  that  time 
free  from  beginning  posterior  spinal  sclerosis,  because  in  the 
routine  examination  for  life  insurance  there  is  no  attempt  at 
examining  for  nervous  symptoms  which  are  not  immediately 
apparent.  On  the  medical  examiner's  blank  the  color  of  the 
eyes  is  noted,  but  there  is  no  space  left  for  statements  con- 
cerning the  condition  of  the  pupils,  and  there  are  no  ques- 
tions relative  to  the  knee-jerk. 

That  an  examination  by  a  competent  physician,  who  is 
also  on  the  alert  for  nervous  disease,  is  necessary  before  any 
one  can  be  pronounced  as  free  from  tabes,  may  seem  equiva- 
lent to  saying  that  all  men  are  ataxic  until  they  are  proved 
not  to  be  so.  Extravagant  as  it  may  appear,  that  such  a  de- 
mand is  essential  in  any  attempts  to  fix  the  beginning  of  the 
disease  will  be  thoroughly  indorsed  by  any  one  who  has 
studied  the  literature  of  the  cases  which  are  said  to  arise 
from  injury,  or  who  has  had  under  his  care  cases  of  tabes 
which  have  remained  for  years  in  the  pre-ataxic  stage,  with 
few  or  no  subjective  symptoms,  but  in  which  symptoms  have 
suddenly  become  active  and  severe  as  a  result  of  some  slight 
injury  or  shock. 


LOCOMOTOR   ATAXIA. 


157 


iEtiology. — It  is  evident  that  there  must  be  considerable 
uncertainty  concerning  the  aetiology  of  a  disease  which  may 
be  in  operation  for  months  or  years  before  its  existence  is 
known.  This  uncertainty  is  not  materially  relieved  b}^  what 
we  know  about  the  causal  agents  of  tabes.  Of  the  various 
ones  which  have  been  named  as  responsible  for  the  spinal 
degeneration,  syphilis  is  least  open  to  destructive  criticism. 
But  even  to  the  influence  of  syphilis  is  attributed  a  differ- 
ent importance  by  various  observers.  Erb  finds  preceding 
syphilis  in  over  ninety  per  cent  of  his  cases  ;  but  of  one  hun- 
dred and  eight  cases  observed  in  Leyden's  clinic,  Storbeck 
finds  only  twenty-three  who  are  surely  syphilitic,  twenty-two 
which  are  doubtful,  and  sixty-three  which  are  "  surely  not 
syphilitic,"  though  how  he  may  be  sure  of  that  is  not  appar- 
ent. However,  all  writers  agree  that  syphilis,  either  as  a 
direct  or  as  a  predisposing  cause,  occupies  a  prominent 
place  among  the  setiological  factors  of  tabes,  although  it  can 
not  be  said  that  tabes  never  develops  unless  the  patient  has 
had  syphilis.  Such  a  possibility  is,  mdeed,  generally  ad- 
mitted, and  Gowers  says  that  in  ten  per  cent  of  the  cases 
syphilis  may  be  excluded  with  confidence. 

Although  there  can  be  no  doubt  as  to  a  relationship  be- 
tween syphilis  and  tabes,  it  is  very  difficult  to  determine 
whether  the  venereal  disease  acts  as  an  exciting  or  as  a  pre- 
disposing cause  of  the  spinal  degeneration.  In  favor  of  the 
theory  that  it  is  an  exciting  cause  is  the  occasionally  observed 
fact  that  tabes  follows  immediately  upon  syphilis  without 
any  other  causes  being  discoverable.  The  evidence  for  it  be- 
ing a  predisposing  cause  is,  in  the  majority  of  cases,  much 
stronger.  Tabes  does  not  usually  appear  until  all  distinctive 
syphilitic  manifestations  have  ceased.  When  syphilitic  and 
tabetic  symptoms  occur  together,  specific  treatment  usually 
causes  the  former  to  subside,  but  has  no  effect  on  the  latter ; 
the  number  of  persons  with  syphilis  is  large,' compared  with 
which    the  number  of    persons  who  develop    tabes  is  ex- 


J  eg  ORGANIC    EFFECTS   OF    INJURY. 

tremely  small ;  the  anatomical  character  of  tabes  is  entirely 
different  from  that  of  recognizable  syphilis.  In  the  cases 
which  are  presumably  free  from  syphilitic  infection,  it  is 
usually  impossible  to  satisfactorily  prove  any  particular  pre- 
disposition to  the  spinal  disease,  or  to  any  disease  of  the 
nervous  system.  Tabes  itself  may  be  said  to  be  never 
directly  transmitted.  Neither  is  the  pathogenesis  of  this 
affection  explained  by  the  other  aetiological  factors.  The 
disease  occurs  chiefiy  in  the  male  sex  (ten  to  one),  and 
most  commonly  appears  in  the  earlier  degenerative  decades 
of  life  (thirty  to  fifty). 

Of  the  various  exciting  causes  which  are  commonly 
mentioned  in  discussions  on  the  etiology,  trauma  is  the 
only  one  of  which  we  need  speak,  except  to  say  of  the 
others  that  their  causal  relationship  to  the  spinal  disease  is 
rarely  clear.  If  trauma  is  a  cause  of  tabes,  what  would  be  its 
most  probable  mode  of  action?  Our  ignorance  concerning 
the  factor  of  predisposition  renders  any  satisfactory  answer 
to  this  question  impossible.  In  the  surely  syphilitic  cases,  if 
the  syphilis  were  considered  an  exciting  cause  of  tabes,  the 
action  of  trauma  could  only  be  regarded  as  an  injurious  in- 
fluence acting  upon  a  disease  which  was  already  inevitable. 
But  if  the  syphilis  had  only  predisposed  the  spinal  cord  to 
degeneration,  it  would  be  entirely  permissible  to  maintain 
that  the  degeneration  would  not  appear  unless  some  excit- 
ing factor  were  added.  Our  ignorance  in  regard  to  the 
nature  of  the  syphilitic  factor,  and  our  total  inability  to  ex- 
plain the  pathogenesis  of  the  cases  in  which  syphilis  proba- 
bly never  existed,  render  it  impossible  to  tell  the  part  that 
trauma  might  play  in  the  evolution  of  tabetic  symptoms 
which  had  been  absent  before  the  injury.  With  a  total 
absence  of  clinical  evidence  adequate  to  determine  the  exist- 
ence of  tabes'  as  a  direct  result  of  injury,  speculations  as  to 
the  possibility  of'such  a  condition  are  more  or  less  futile.  If 
it  is  permissible  to  reason  from  analogy  and  from  the  study 


LOCOMOTOR   ATAXIA. 


159 


of  those  cases  published  as  traumatic,  in  which,  although 
they  are  incomplete  as  evidence,  the  influence  of  trauma  in  the 
development  of  the  disease  can  not  be  denied,  it  would  seem 
that,  if  tabes  is  to  result  from  injuries  at  all,  it  will  be  found 
to  be  from  injuries  to  the  peripheral  nerves.  It  has  been 
shown  by  Soukanoff  and  others  that  posterior  spinal  degen- 
eration not  infrequently  develops  from  disorders  which 
originally  were  clinically  typical  of  multiple  nerve  inflamma- 
tion. Now,  most  of  the  cases  of  tabes  reported  as  traumatic, 
which,  although  they  do  not  prove  a  traumatic  origin  for  the 
disease,  might  have  been  traumatic,  have  developed  after  gun- 
shot or  other  wounds  of  the  limbs,  which  may  have  involved 
the  nerves.  It  may  be  possible  that  injury  to  a  peripheral 
nerve  can  cause  a  neuritis  which  ascends  to  the  posterior 
spinal  ganglion,  inducing  disturbances  there  that  are  to  be- 
come the  starting  points  of  degeneration  in  the  spinal  cord. 
Such  a  view  of  pathogenesis  is  however  purely  speculative. 

If  trauma  stands  in  any  causal  relation  whatsoever  to  tabes, 
such  a  connection  must  be  very  infrequent.  Of  two  hundred 
and  eighty-one  cases  of  Erb,  trauma  is  mentioned  as  a  sole 
cause  in  only  one.  Now,  tabes  has  received  more  careful 
attention  than  almost  any  other  disease  of  the  nervous  sys- 
tem, and  several  monographs  appear  every  year  on  Eetiology 
alone.  Yet,  among  the  thousands  of  cases  which  have  been 
reported  in  detail,  there  are  only  a  few  dozen  which  are 
alleged  to  have  been  solely  due  to  injury.  Of  the  one 
hundred  and  eighty-five  full  clinical  histories  of  the  disease 
which  are  recorded  in  the  books  at  the  Vanderbilt  Clinic,  in 
three  cases  only  is  there  mention  of  an  injury  which  might 
be  regarded  as  causal:  of  these,  one,  with  the  Charcot  joint 
has  already  been  mentioned  ;  in  another,  there  was  an  inter- 
val of  twenty-nine  years  between  the  occurrence  of  the  acci- 
dent and  the  first  appearance  of  spinal  symptoms.  The 
third  is  unique,  and  since  it  presents  such  evidences  as 
would  be  accepted  as  final  by  any  one  unfamiliar  with  the 


i6o 


ORGANIC  EFFECTS  OF  INJURY. 


insidious  character  of  the  onset  of  the  disease,  it  must  be 
recorded  in  detail  : 

The  patient,  a  railway  employee,  thirty-nine  years  of  age,  fell 
off  a  freight  car  in  October,  1896,  striking  on  his  buttocks  and  sus- 
taining a  fracture  of  the  pelvis  and  some  injury  to  the  left  leg.  For 
one  month  he  was  in  bed  in  the  hospital,  bolstered  up  with  sand  bags, 
with  an  extension  splint  on  the  left  leg.  Then  he  got  up,  and  in  try- 
ing to  walk  around  his  bed  fell  to  the  floor  and  sustained  another 
fracture.  He  was  in  bed  again  for  four  weeks,  and  when  he  got  up 
this  time  found  he  could  not  use  his  legs  properly,  a  condition  which 


270  270 

Fig.  37. — Field  of  vision  in  a  case  of  locomotor  ataxia  which  developed  immediately 
after  an  injury.     (Vanderbilt  Clinic.) 

has  remained  about  stationary.  He  came  to  the  Vanderbilt  Clinic 
in  July,  1897,  presenting  the  ordinary  symptoms  of  locomotor  ataxia 
— viz.,  ataxia  and  loss  of  muscular  sense  in  the  legs,  without  motor 
paralysis,  Romberg  symptom,  loss  of  knee-jerks,  difficulty  in  pass- 
ing water,  and  numbness  in  the  legs  (no  objective  anaesthesia).  The 
left  pupil  was  larger  than  the  right  and  responded  slightly  during 
efforts  at  accommodation,  but  not  to  light.  The  right  pupil  was 
immobile.  Vision:  R.  E.,  f^  ;  L.  E.,  ff  (for  field  of  vision  see 
Fig-  37).  The  ophthalmoscope  showed  pronounced  optic-nerve 
atrophy  in  both  eyes,  most  marked  on  the  right  side. 

When  questioned  as  to   possible  causes,  the  patient  made  the 
following  replies : 


LOCOMOTOR   ATAXIA.  l6l 

Syphilis. — He  denied  emphatically  every  symptom  of  any  vene- 
real disease.  He  was  married  at  the  age  of  twenty-four,  and 
his  wife  gave  birth  to  two  healthy  children.  One  miscarriage 
came  at  the  eighth  month,  but  it  followed  immediately  upon  a 
fall,  and  consequently  can  not  be  regarded  as  an  evidence  of 
syphilis. 

Condition  Previous  to  the  Injury. — The  patient  could  not  be 
made  to  admit  the  existence  of  any  tabetic  symptom  previous 
to  the  injury.  He  was  positive  that  he  had  never  had  any  diffi- 
culty in  walking,  either  on  the  street,  on  the  stairs,  or  in  the 
dark ;  he  did  not  fall ;  he  never  had  shooting  pains.  He  said 
that  for  several  years  before  the  accident  his  eyesight  had  not 
been  so  good  as  formerly,  but  he  could  read  the  paper  without 
difficulty,  and  that  three  or  four  months  before  the  accident  he  suc- 
cessfully passed  the  examination  of  the  eyes  for  color  perception, 
which  was  demanded  by  the  railway  of  which  he  was  an  employee. 
He  stated  that  many  of  the  employees  were  rejected  at  this  ex- 
amination. 

After  the  Accident. — The  first  symptom  he  observed  was  fail- 
ure of  sight.  In  a  week  or  ten  days  after  he  had  been  in  the 
hospital  his  vision  became  so  poor  that  he  could  no  longer  read 
the  paper,  and  since  then  he  has  been  unable  to  read  any  but  very 
large  type.  The  other  symptoms  of  tabes  were  only  observed 
when  he  left  the  bed,  and  are  essentially  those  which  have  been 
enumerated.  The  patient  had  never  thought  of  bringing  a  claim 
against  the  company,  and  his  whole  manner  spoke  agauist  his  hav- 
ing any  desire  or  motive  for  telling  anything  but  the  truth. 

Thus  an  apparently  healthy  man,  not  predisposed  to  nervous 
disease,  receives  an  injury  and  rapidly  develops  symptoms  of 
locomotor  ataxia.  The  accident  might  be  regarded  as  the  sole 
cause,  were  it  not  that,  on  account  of  the  latent  character  of  the 
disease,  no  injury  can  be  said  to  be  causal,  unless,  previously  to 
its  receipt,  tabetic  symptoms  were  shown  to  be  absent. 

In  spite  of  the  absence  of  adequate  and  reasonable  proof, 
in  most  text-books  on  nervous  diseases  trauma  receives  an 
important  place  among  the  exciting-  causes  of  the  disease. 
For  purposes  of  scientific  interest  and  also  because  in 
negligence  cases  injury  may  be  alleged  to  be  the  cause  of 
the  disease  by  persons  w^ho,  though  honest,  are  ignorant  of 
symptomatology,  or  by   persons   with  fraudulent  intent,  it 


l62  ORGANIC    EFFECTS   OF   INJURY. 

is  very  essential  that  the  merits  of  the  question  be  clearly 
understood. 

The  subject  has  received  careful  study  by  Prince,  who 
criticises  all  previously  reported  cases  with  a  view  of  deter- 
mining if  in  any  case  the  disease  could  have  been  reasonably 
presumed  to  be  of  traumatic  origin. 

He  analyzed  the  forty  cases  of  tabes  which  had  been  pub- 
lished as  traumatic,  and  rejected  them  all  as  being  insuf- 
ficient as  evidence,  although  he  admits  that  twelve  of  them 
might  have  been  of  traumatic  origin.  But  not  a  single  case 
fulfills  satisfactorily  the  conditions  which  must  be  com- 
plied with  if  we  are  to  insist  on  anything  like  reasonable 
proof. 

The  most  important  of  these  conditions  is  to  show  that 
tabes  had  not  pre-existed.  If  this  can  not  be  done,  the  in- 
sidious character  of  the  disease  would  place  the  weight  of 
evidence  with  him  who  claimed  that  it  had  antedated  the 
accident.  As  has  already  been  indicated,  such  proof  is  usu- 
ally lacking,  yet  without  it  any  claim  of  tabes  caused  by 
injury  lacks  basis.  Prince  expresses  the  opinion,  which  is 
indorsed  by  Bernhardt,  that  tabes  can  not  be  regarded  as 
traumatic  if  the  patient  has  had  syphilis.  Inasmuch  as  we 
are  ignorant  of  how  syphilis  acts  in  the  setiology  of  the 
spinal  disease,  and  in  the  absence  of  proof  that  injury  can 
cause  tabes  in  syphilitic  persons,  this  view  appears  unwar- 
rantable. In  regard  to  the  severity  and  character  of  the 
injury  we  are  equally  in  the  dark.  It  is  generally  un- 
profitable to  speculate  as  to  how  the  human  body  will  react 
to  injurious  influences  if  we  have  no  clinical  data  upon 
which  to  rely. 

From  general  principles  it  would  seem  reasonable  to 
expect  that  an  injury  to  cause  so  general  a  disease  as  tabes 
would  have  to  be  physical  and  reasonably  severe.  Psychic 
shock  seems  hardly  sufficient  to  induce  nerve  degeneration. 

To  be  serviceable  as  evidence,  the  interval  between  the 


LOCOMOTOR    ATAXIA.  l5^ 

receipt  of  the  trauma  and  the  first  appearance  of  symptoms 
would  have  to  be  no  longer  than  a  few  weeks  or  months. 
If  tabes  results  from  nerve  injuries,  the  interval  should  be 
occupied  by  symptoms  of  neuritis. 

Since  the  writing  of  Prince's  paper  three  other  cases 
have  been  reported.  In  one,  by  Bernhardt,  tabes  had  ex- 
isted before  the  injury,  but  had  been  made  worse  by  it;  in 
another,  by  Hitzig,  there  was  no  examination  until  a  year 
and  a  half  after  the  accident ;  and  in  one,  by  Craig,  there 
seems  to  have  been  some  doubt  as  to  the  correctness  of  the 
diagnosis  of  tabes. 

Thus  the  matter  stands  as  it  did  in  1895,  and  we  can  do 
no  better  than  to  repeat  the  conclusion  of  Prince,  that  "  the 
view  that  locomotor  ataxia  may  be  caused  by  traumatism 
per  se,  irrespective  of  a  direct  lesion  of  the  cord,  is  not  sus- 
tained by  the  published  evidence  thus  far  adduced.  If  such 
a  relation  exists,  further  evidence  is  required  before  it  can 
be  accepted." 

It  seems  as  though  Prince  would  have  been  justified  in 
going  even  still  further,  and  in  saying  that,  in  view  of  the 
large  number  of  published  cases  of  tabes,  compared  with  the 
few  cases  reported  as  traumatic,  and  in  the  total  absence  of 
any  verification  of  traumatism  as  a  cause,  it  is  improbable 
that  injury  or  shock  stand   in  any  direct  causal   relation  to 

the  disease. 

Bibliography. 

Bernhardt,  Zur  Lehre  von  der  traum.  Tabes.  Monats.f.  Un- 
fallheilkunde,  1895,  vol.  ii,  p.  193. 

Craig,  Case  of  Tabes  from  Injury.     Lancet,  1895,  vol.  i.  No.  8. 

Erb,  Syphilis  and  Tabes.     Berl.  klinische  Woch.,  1896,  No.  11. 

Hitzig,  Ueber  traum.  Tabes  u.  d.  Pathogenese  der  Tabes  im 
Allgemeine.     Berlin,  1894. 

■     Prince,  Traumatism  as  a  Cause  of  Locomotor  Ataxia.     Jour. 
Nerv.  and  Mejit.  Dis.,  February,  1895. 

Storbeck,  Tabes  Dors,  und  Syphilis.    Inaug.  Diss.,  Berlin,  1895. 

Soukanoff,  Contribution  a  I'etude  des  changements  du  systeme 
nerveux  dans  la  polynevrite.     Arch,  de  neuroL,  1896,  p.  177. 


A^ 


j54  organic  effects  of  injury. 

Progressive  Muscular  Atrophy  (Creeping  Palsy). 

Including  Amyotrophic  Lateral  Sclerosis. 

The  researches  of  recent  years  have  very  much  enlarged 
the  field  occupied  by  the  disorders  in  which  wasting  of  the 
muscles  occurs,  so  that  to-day  the  term  progressive  muscu- 
lar atrophy  might  be  construed  so  as  to  include  atrophies 
which  are  progressive,  although  different  in  course  and  pa- 
thology from  the  original  disorder  described  by  Duchenne. 
There  are  at  present  two  distinct  and  well-recognized  groups 
of  muscular  atrophies,  one  of  which  is  spinal  in  origin,  and 
the  other  of  which  commences  in  and  remains  localized  to 
the  muscles  without  any  involvement  of  the  spinal  cord. 
The  latter  variety,  more  commonly  called  progressive  mus- 
cular dystrophy,  occurs  in  families,  is  a  disease  of  childhood 
and  youth,  has  a  different  muscular  localization  from  the 
spinal  type,  and,  as  it  is  rarely  if  ever  suspected  of  being  of 
traumatic  origin,  requires  no  mention  here. 

The  most  prominent  anatomical  feature  of  progressive 
muscular  atrophy  (spinal)  is  a  degeneration  in  all  parts  of 
the  peripheral  motor  neuron,  with  a  resulting  wasting 
of  the  muscles.  Associated  with  the  degeneration  of  the 
peripheral  neural  element  there  almost  constantly  occur  de- 
generative changes  in  the  lower  portion  of  the  central  neu- 
ron, which  descends  from  the  cortex  in  the  motor  tract,  and 
which  is  continued  through  the  spinal  cord  in  the  pyrami- 
dal tracts. 

According  as  the  morbid  changes  are  most  pronounced 
in  one  or  the  other  of  these  two  neurons,  the  clinical  type 
of  the  disease  varies.  (Compare  page  55.)  Thus,  if  the 
primary  (or  peripheral)  neuron  is  chiefly  affected,  the  atro- 
phy and  weakness  will  be  extreme  and  reflex  irritability  will 
be  lost,  in  accordance  with  the  type  of  pure  atrophic  paral- 
ysis. On  the  other  hand,  if  it  is  the  pyramidal  tracts  which 
are  the  more  involved,  the  character  of  the  paralysis  will  be 


PROGRESSIVE    MUSCULAR   ATROPHY. 


165 


spastic,  with  a  certain  rigidity  of  the  muscles  and  an  in- 
crease  of  the  tendon  reflexes. 

To  the  spastic  form  of  progressive  muscular  atrophy  has 
been  given  the  name  of  amyotrophic  lateral  sclerosis.  It  is 
a  convenient  clinical  term,  but,  in  spite  of  a  recent  mono- 
graph by  J.  B.  Charcot  in  defense  of  its  autonomy,  I  have 
been  unable  to  convince  myself  that  any  differentiation  of 
the  two  conditions  is  justifiable  on  anatomo-pathological 
grounds.  In  by  far  the  larger  number  of  cases  there  are 
morbid  changes  both  in  the  anterior  horns  and  in  the  pyrami- 
dal tracts,  and  the  clinical  differences  which  are  observed, 
according  as  one  or  the  other  neuron  is  the  more  affected, 
seem  to  be  variations  from  a  common  condition,  rather 
than  expressions  of  separate  morbid  entities.  Accordingly, 
in  speaking  of  the  traumatic  origin  of  progressive  muscular 
atrophy,  the  term  will  be  used  so  as  to  include  the  clinical 
type  known  as  amyotrophic  lateral  sclerosis. 

Symptoms. — The  symptoms  of  progressive  muscular 
atrophy  consist  of  atrophy,  weakness,  and  fibrillation  of  the 
affected  muscles,  with,  in  the  early  stages,  a  slight  alteration 
of  electrical  excitability  only.  Objective  sensory  symptoms 
are  never  prominent,  but  there  may  be  pain,  especially  if 
the  process  is  rapid.  Pain  has  usually  been  mentioned  when 
the  disorder  has  followed  traumatism.  The  bladder  and  the 
rectum  are  rarely  involved  in  this  disease,  and  there  is  al- 
most never  complete  loss  of  sphincter  control. 

The  symptoms  vary  with  the  locality  of  the  lesion, 
and  several  types  have  been  described  which  depend  for 
their  individuality  upon  the  situation  of  the  muscles  that 
are  first  attacked.  The  type  Duchenne-Aran  is  by  far  the 
most  frequent.  In  it  the  locations  in  which  the  disease  first 
appears  and  the  order  in  which  it  progresses  are  fairly  con- 
stant. Beginning  on  one  side  in  the  muscles  at  the  base  of 
the  thumb,  and  in  the  interossei,  it  skips  up  to  the  shoulder 
to  affect  the  deltoid  and  perhaps  others  of  the  shoulder  mus- 


l66  ORGANIC  EFFECTS  OF  INJURY. 

cles.  The  muscles  of  the  arm  and  forearm  may  next  be  in- 
volved, or  the  disease  may  first  pursue  in  the  upper  extrem- 
ity of  the  opposite  side  the  same  course  that  it  followed  in 
the  extremity  first  attacked.  Very  frequently  the  deltoid 
is  the  earliest  to  waste,  the  small  muscles  of  the  hand 
joining-  in  the  atrophy  at  a  later  period.  In  more  advanced 
stages  the  process  may  move  upward,  giving  the  picture  of 
glosso-labio-pharyngeal  paralysis,  or  it  may  descend  to  in- 
volve the  legs. 

A  less  frequent  type  of  progressive  muscular  atrophy  is 
the  "  peroneal,"  called,  after  its  earliest  describers,  the  Tooth 
or  Charcot-Marie  type.  Its  pathology  is  obscure,  as  it  still 
remains  to  be  conclusively  proved  that  it  depends  upon  dis- 
ease of  the  anterior  horns  of  the  spinal  cord. 

The  course  of  progressive  muscular  atrophy  is  chronic, 
although  very  much  more  rapid  than  that  of  locomotor 
ataxia.  In  many  cases  the  progress  becomes  slower  as  the 
disease  advances,  and  in  some  it  seems  to  stop  altogether. 
When  complicated  by  bulbar  palsy,  death  soon  ensues  from 
failure  of  respiration,  or  from  "  foreign  body  "  pneumonia. 
If  the  atrophy  remains  limited  to  the  hand  and  shoulder 
muscles,  the  patient  may  live,  incapacitated,  for  many 
years. 

iEtiology. — Even  less  is  known  about  the  causation  of 
progressive  muscular  atrophy  than  about  that  of  tabes.  Syph- 
ilis is  spoken  of  as  a  cause,  but  its  influence  is  not  proved,  and 
is  certainly  very  much  less  important  than  in  tabes.  Exposure 
to  cold  and  wet,  and  overexertion  have  sometimes  preceded 
the  first  appearance  of  the  disease.  From  the  fact,  as  first 
shown  by  Ballet  and  Dutil  and  later  by  Hirsch,  that  the 
chronic  disease  may  first  appear  in  muscles  which  had  been 
afTected  by  acute  infantile  spinal  palsy,  it  seems  as  though 
preceding  inflammatory  conditions  of  the  spinal  cord  might 
be  a  predisposing  cause. 

The  causal  relation  of  traumatism  to  progressive  muscu- 


PROGRESSIVE    MUSCULAR   ATROPHY.  167 

lar  atrophy  is  fairly  well  established.  A  considerable  num- 
ber of  cases  are  on  record  in  which  injury  of  a  limb  was 
quickly  followed  by  an  atrophy  of  its  muscles,  a  condition 
which  later  became  general. 

Less  frequently  blows  on  the  back  or  concussion  acci- 
dents have  been  the  only  discoverable  cause  of  the  typical 
symptoms  which  shortly  after  ensued. 

Diagnosis. — To  prove  progressive  muscular  atrophy  to 
be  in  all  probability  the  result  of  injury  it  must  be  shown : 
I.  That  the  patient  has  muscular  atrophy.  2.  That  he  were 
free  from  the  disease  a  short  time  before  or  immediately 
after  the  accident.  3.  That  the  accident  caused  a  consider- 
able shaking  of  the  body  or  injury  to  a  limb. 

I.  The  first  requirement  is  a  question  of  diagnosis,  about 
which  there  is  usually  little  difficulty.  If  the  disease  is  of 
the  lower  Duchenne-Aran  type,  the  two  conditions  to  be 
eliminated  are  injury  to  the  ulnar  nerve  and  lead  palsy.  It 
will  be  remembered  that  the  ulnar  nerve  supplies  the  inter- 
osseous muscles  and  that  injury  to  it  causes  main  en  griff e, 
which  is  also  a  frequent  symptom  in  progressive  muscular 
atrophy.  If  the  history  told  by  the  patient  is  reliable,  ulnar 
nerve  palsy  and  progressive  muscular  atrophy  will  rarely  be 
confused.  In  the  peripheral  lesion  the  atrophy  develops 
very  much  more  rapidly,  the  loss  of  muscular  power  is 
greater,  and  the  subjective  sensory  sensations  are  more 
prominent.  The  diagnosis  may,  however,  usually  be  made 
by  objective  signs  alone.  In  any  palsy  of  a  peripheral  nerve 
which  is  sufficiently  severe  to  cause  pronounced  atrophy, 
the  electrical  conductivity  of  the  nerve  is  very  much  dimin- 
ished or  lost.  In  nerve  injuries  without  severe  wounds  or 
fractures,  fibrillary  twitchings  are  not  marked,  and  in  an  in- 
jury to  the  ulnar  nerve  there  is  never  any  involvement  of 
the  deltoid. 

The  differentiation  from  lead  palsy  may  be  more  difficult. 
If  there  are  no  constitutional  evidences  of  plumbism,  it  is 


1 68  ORGANIC  EFFECTS  OF  INJURY. 

sometimes  an  exceedingly  delicate  matter  to  decide  between 
lead  palsy  and  a  progressive  muscular  atrophy  in  which  the 
extensors  of  the  wrist  and  fingers  have  become  involved  on 
both  sides.  In  lead  palsy  the  supinator  longus  and  the  ex- 
tensor ossis  metacarpi  poUicis  escape.  But  they  may  also  be 
the  only  muscles  to  escape  in  the  spinal  disease.  In  a  recent 
case  at  the  Vanderbilt  Clinic,  in  which  the  wasting  and 
paralysis  were  bilateral  and  which  by  its  course  has  been 
proved  to  be  one  of  progressive  muscular  atrophy,  these 
two  muscles  were  the  only  ones  of  the  extensor  group  which 
had  not  been  involved  by  the  paralysis.  Such  cases,  how- 
ever,  are  unusual ;  most  frequently  progressive  muscular 
atrophy  is  at  first  unilateral,  or  very  much  more  marked  on 
one  side  than  on  the  other.  If  it  has  developed  in  both 
hands,  there  are  also  characteristic  atrophies  about  the 
shoulder  muscles,  the  extensors  of  the  wrist  not  being 
affected  until  a  later  period  of  the  disease. 

If  traumatic  progressive  muscular  atrophy  begins  in  the 
deltoid  or  other  of  the  shoulder  muscles,  it  may,  if  the  his- 
tory be  unreliable,  be  confused  with  some  of  the  palsies  of 
the  brachial  plexus.  The  distribution  of  the  palsy  and  the 
results  of  electrical  examination,  as  indicated  in  Chapter  III, 
will  usually  permit  a  recognition  of  the  two  conditions.  In- 
crease of  the  tendon  reflexes,  both  at  the  knee  and  in  the 
upper  extremity,  frequently  occurs  in  progressive  muscular 
atrophy,  but  is  never  a  part  of  the  peripheral  disorder  with 
which  it  might  be  confused.  Its  existence  is  therefore  a 
valuable  aid  in  diagnosis. 

2.  The  validity  of  a  claim  of  progressive  muscular  atro- 
phy caused  by  injury  depends  very  largely  upon  the  ability 
of  the  claimant  to  prove  himself  to  have  been  free  from  the 
disease  at  the  time  of  the  accident.  Such  proof  is  more 
easily  attainable  than  it  is  for  the  tabetic  to  prove  that  at 
any  given  time  he  had  no  symptoms  of  tabes  ;  for  the 
symptoms  of  progressive  muscular  atrophy  are  nearly  alto- 


PROGRESSIVE    MUSCULAR   ATROPHY.  i6q 

g-ether  objective,  and  are  of  a  character  to  be  noticed,  not 
only  by  the  patient  but  by  his  friends.  A  marked  sinking- 
in  between  the  first  finger  and  thumb  may  occur  in  a 
month's  time,  and  although  the  atrophy  is  usually  more 
rapid  in  its  development  than  the  loss  of  power,  even  a 
weakness  of  the  interossei  is  so  annoying  and  disabling,  and 
causes  so  serious  an  impairment  of  those  finer  movements 
of  the  fingers  which  are  essential  for  the  commonest  daily 
duties,  that  it  could  not  exist  without  becoming-  the  subject 
of  remark.  If  a  person  who  develops  soon  after  an  accident 
progressive  muscular  atrophy,  type  Duchenne-Aran,  could 
prove  that  he  had  continued  to  do  manual  work  satisfac- 
torily up  to  the  time  of  the  injury,  it  would  be  very  good 
evidence  that  he  were  then  at  least  free  from  the  disease. 
In  most  of  the  reported  traumatic  cases  the  patients  were 
active  workers  up  to  the  time  of  injury. 

3.  The  accident  which  has  most  frequently  induced  the 
disease  has  usually  been  severe.  I  know  of  no  case  in  which 
fright  alone  is  said  to  have  been  a  cause,  and  in  most  the  in- 
jury  was  very  appreciable. 

Illustrative  Cases. — The  kind  of  accident  and  the  mode 
of  the  first  appearance  of  symptoms  may  be  illustrated  by 
the  following  cases  ;  some  have  been  seen  at  the  Vanderbilt 
Clinic,  and  others  are  derived  from  various  sources.  For 
two  reasons  no  effort  has  been  made  to  include  all  the  cases 
published  as  due  to  traumatism  :  First,  because  the  clinical 
evidence  in  favor  of  a  traumatic  origin  of  the  disease  is  too 
well  established  to  make  such  a  review  necessary  ;  and,  sec- 
ondly, because  many  of  the  cases  have  been  described  in  a 
way  that  renders  it  impossible  for  the  reader  to  determine 
whether  the  disease  had  been  caused  by  injury,  or  whether, 
indeed,  it  were  unquestionably  progressive  muscular  atro- 
phy. The  following  cases,  therefore,  have  been  chosen,  in- 
asmuch as  they  seem  to  prove  with  a  considerable  degree  of 
probability  that  progressive  muscular  atrophy  may   result 


J-70  ORGANIC    EFFECTS    OF    INJURY. 

from  injury,  and  because  they  illustrate  the  clinical  courses 
of  such  cases : 

Raymond  quotes  from  Friedreich  the  case  of  a  man  who, 
after  a  bruise  of  the  right  hand,  developed  an  atrophy  in 
that  hand  which  followed  a  progressive  and  ascending 
course  and  was  eventually  complicated  by  bulbar  palsy. 
He  also  refers  to  Poncet's  report  of  a  soldier  who  was  shot 
in  the  right  shoulder.  The  muscles  of  the  wounded  shoul- 
der soon  became  atrophied  and  the  left  shoulder  became  in- 
volved later. 

Clarke  describes  a  case  which,  in  addition  to  furnishing 
a  good  example  of  traumatic  progressive  muscular  atrophy, 
illustrates  the  predisposing  influences  of  certain  occupations, 
and  shows  the  injurious  effect  of  depressing  mental  influ- 
ences upon  the  course  of  the  spinal  disease  : 

A  woman,  thirty-eight  years  of  age,  married,  seamstress,  of  deli- 
cate constitution,  fell  downstairs  and  hurt  her  right  hand  and 
especially  the  thumb.  One  year  later  there  was  pain  in  the  right 
arm,  neck,  and  shoulder.  She  was  unable  to  hold  her  needle,  yet 
there  was  no  pain  in  the  hand  or  forearm.  At  this  time  the  mus- 
cles of  the  arm  and  forearm  began  to  waste,  but  improved  again 
in  two  months.  The  sudden  death  of  her  husband  caused  her  a 
severe  mental  shock,  and  she  then  complained  of  pain  in  the  neck 
and  that  both  the  arms  and  both  the  legs  felt  weak,  cold,  and 
sometimes  numb.  Loss  of  power  of  the  neck  muscles  ensued,  and 
the  right  arm  soon  became  almost  completely  useless. 

When  admitted  to  the  hospital  the  right  arm  was  paralyzed  and 
wasted,  and  the  examiner  "  could  feel  only  fat,  skin,  and  bones." 
No  reaction  to  faradism.     No  stiffness. 

Examination. — Left  arm  :  Little  power  in  the  hand.  The  pa- 
tient can  extend  the  fingers  slowly  and  feebly.  All  the  thurnb 
muscles  are  wasted.  The  muscles  of  the  lower  two  thirds  of  the 
forearm  are  wasted,  as  are  the  supinators.  She  can  wriggle  the 
arm  along  the  chest.  There  is  a  fair  quantity  of  muscle  on  the 
upper  arm.    Interossei  react  to  a  slight  current ;  extensors  feebly. 

Neck  :  Muscles  can  only  bend  the  head  a  little.  There  is  slight 
power  in  the  left  trapezium,  but  none  in  the  right.  Muscles  on  the 
scapulae  are  gone.  The  facial  muscles  act  slightly.  Palate  moves 
slightly.     Tongue  protrudes,  but  is  atrophied  on  both  sides.     Deg- 


PROGRESSIVE    MUSCULAR   ATROPHY. 


171 


lutition  imperfect.  The  right  leg  is  wasted,  but  retains  slight 
power  of  movement.  There  is  considerable  strength  in  the  left 
leg.  Patient  died  four  months  after  admission  to  the  hospital,  and 
about  two  years  (?)  after  the  receipt  of  the  injury. 

A  case  of  the  late  Prof.  Eisenlohr's  is  interesting,  as  it 
shows  the  early  appearance  of  the  symptoms  of  bulbar  palsy 
after  an  injury  to  the  upper  part  of  the  spinal  column,  and 
follows  the  clinical  type  of  amyotrophic  lateral  sclerosis  in 
the  extremities  : 

A  locksmith,  forty-nine  years  of  age,  asserts  that  he  had  been 
well  previously  to  the  receipt  of  a  blow  on  the  neck  in  the  spring 
•of  1877.  In  July  of  the  same  year  there  appeared  a  gradual  weak- 
^ness  of  the  arms  and  hands,  which  extended  two  months  later  to 
the  legs.  In  October  began  disturbances  of  articulation.  Exami- 
nation in  January,  1878,  showed  the  following  conditions  : 

The  lower  part  of  the  face  is  flaccid,  the  lips  are  constantly 
•open,  and  blowing  and  whistling  are  impossible. 

The  tongue  is  atrophic  and  its  movements  are  limited.  The 
articulation  of  all  consonants  is  bad. 

Movements  of  the  soft  palate  are  very  slow.  Swallowing  and 
chewing  normal.  The  shoulder  and  upper  arm  muscles  are  mod- 
erately atrophied  on  both  sides.  The  muscles  of  the  forearm  are 
markedly  atrophied  on  both  extensor  and  flexor  surfaces,  the  in- 
terosseous spaces  of  both  hands  are  deeply  sunken  in,  and  the 
thenar  and  hypothenar  eminences  are  flattened.  The  hands  and 
fingers  are  almost  immobile.  Great  loss  of  power  in  both  arms. 
Sensibility  is  normal.  The  reflexes  are  active.  Electrical  excita- 
bility is  diminished.  Similar  changes,  though  less  marked,  are  ob- 
•served  in  the  lower  extremities. 

Death  occurred  in  a  few  months  as  the  result  of  the  bulbar 
palsy.  The  autopsy  and  subsequent  microscopical  examination 
showed  a  degeneration  of  the  anterior  horns  of  the  spinal  cord 
and  of  both  pyramidal  tracts. 

Progressive  muscular  atrophy  sometimes  results  from 
head  injury,  or  at  least  from  accidents  in  which  the  head,  was 
injured.  In  such  cases  there  has  usually  been  considerable 
general  violence,  and  it  is  impossible  to  tell  how  much  of  it 
has  been  exerted  on  the  spine. 


1^2  ORGANIC  EFFECTS  OF  INJURY. 

Mann  reports  the  case  of  an  Englishman  who  at  the  age  of 
twenty-one  fell  from  the  rigging  to  the  deck  of  a  ship.  He  was 
rendered  unconscious  but  sustained  no  fractures  of  the  bones. 
Previously  to  this  accident  the  patient  had  been  perfectly  well. 
Denied  syphilis  or  nervous  disease  in  his  ancestors.  One  month 
after  the  fall  the  deltoid  began  to  waste,  then  the  biceps  and  the 
lower  arm  muscles,  and  finally  the  muscles  of  the  legs.  One  year 
later  he  was  seen  by  Sir  William  Gull,  who  thought  the  patient 
could  not  live  twelve  months.  The  disease  came  to  a  standstill,, 
however,  for  seventeen  years  after  the  accident  the  patient  was. 
treated  by  Dr.  Mann  for  another  condition. 

In  a  case  of  Bullard's,  a  teamster,  sixty-one  years  of  age,. 
a  staging  fell  and  struck  the  side  of  his  head. 

The  patient  had  been  in  previous  good  health ;  there  was  nO' 
syphilis  or  rheumatism  or  other  causes  of  constitutional  disease 
discoverable,  although  signs  of  phthisis  appeared  while  the  patient 
was  under  observation. 

There  was  no  loss  of  consciousness  at  the  time  of  the  accident, 
but  soon  after  it  the  patient  felt  pains  in  the  head,  neck,  and  left 
shoulder,  which  were  followed  by  weakness  and  atrophy  of  the 
muscles  of  the  left  arm  and  hand.  Seven  months  after  the  injury 
he  was  first  seen  by  Dr.  Bullard.  The  muscles  of  the  shoulder  and 
of  the  back  on  the  left  side  were  markedly  atrophied,  those  of  the 
upper  arm  less  so.  The  forearm  was  still  less  affected.  Main  en 
griffe.  Thenar  and  hypothenar  eminences  flattened.  In  the  in- 
terossei  there  was  diminished  faradic  reaction.  Fibrillary  twitch- 
ings  were  marked.  The  patient  gradually  grew  worse  and  the  left 
arm  became  affected.  One  year  later  the  atrophy  in  the  muscles- 
of  the  upper  part  of  the  back  and  the  fibrillary  twitchings  became 
very  marked.  Reaction  to  faradism  was  diminished,  but  sensation 
remained  normal. 

A  case  by  Ziehen  is  less  convincing  : 

Man,  twenty-one  years  of  age,  healthy,  received  a  severe  blow 
in  the  chest  and  was  then  thrown  into  a  ditch,  where  he  lay  un- 
conscious for  some  time.     This  was  in  March,  1888. 

He  suffered  from  fatigue  off  and  on,  which  was  increased  on 
one  occasion  especially  when  he  stood  for  some  hours  in  the  river 
fishing  (in  July,  1889).  He  soon  became  unable  to  do  heavy  work, 
and  appeared  at  the  clinic  in  1890,  showing  a  well-advanced  case 
of  progressive  muscular  atrophy. 


PROGRESSIVE    MUSCULAR   ATROPHY.  173 

Ziehen  maintains  that  the  atrophy  was  caused  by  the  original 
injury,  and  that  the  standing  in  cold  water  only  aggravated  a 
process  which  had  become  established.  The  interval  of  time, 
however,  which  elapsed  between  the  accident  and  the  date  of  the 
medical  examination  was  too  long  to  permit  an  inference  of  any- 
thing more  than  a  possible  relation  between  the  original  trauma 
and  the  spinal  disease. 

The  relationship  between  preceding  inflammations  and 
the  development  of  progressive  muscular  atrophy  is  shown 
by  the  following  case  : 

An  electric  lineman,  thirty-five  years  of  age,  a  steady  drinker, 
who  had  had  the  initial  lesion  of  syphilis  in  1885,  came  to  the 
Vanderbilt  clinic  on  October  30,  1896.  He  said  that  in  1888  he 
fell  forty  feet  from  a  pole,  landing  on  the  back  and  buttocks.  He 
then  walked  a  few  steps,  but  his  legs  soon  gave  out  from  under  him 
and  he  was  carried  to  bed,  completely  disabled  in  the  lower  ex- 
tremities. For  three  months  he  was  in  bed,  unable  to  move  his 
legs.  The  urine  had  to  be  drawn  with  a  catheter.  He  then  re- 
covered and  went  back  to  work,  and  continued  at  work  until  July, 
1896.  He  told  us  that  for  the  past  three  months  he  had  noticed  a 
gradually  increasing  weakness  in  the  legs  and  thighs,  without  pain, 
but  with  soreness  across  the  back  and  stiffness  at  the  ankle,  hip, 
and  knee  joints;  paraesthesia  existed  in  the  sole  of  the  left  foot 
and  in  the  ulnar  distribution  of  the  fingers,  with  considerable 
weakness  in  the  left  arm— a  condition  which  was  also  just  com- 
mencing to  be  felt  in  the  right  hand. 

Examination. — Gait  is  paretic  and  spastic ;  there  is  atrophy 
of  the  right  calf  muscles,  less  marked  on  the  left  side.  Double 
ankle  clonus  and  exaggerated  knee-jerks.  Atrophy  of  the  first 
interossei  muscles  of  both  hands  and  beginning  main  en  griffe. 
Fibrillary  twitchings  on  the  inner  sides  of  both  arms. 

At  the  time  of  the  examination  the  patient  was  a  good  illustra- 
tion of  the  peroneal  type  of  progressive  muscular  atrophy.  The 
atrophy  and  loss  of  power,  which  had  begun  and  remained  most 
marked  in  the  legs,  had  already  involved  the  small  muscles  of  the 
upper  extremities.  If  one  be  permitted  to  speculate  as  to  the 
probable  genesis  of  the  disorder,  it  would  seem  not  improbable 
that  the  original  injury  (in  1888),  coming  so  soon  after  the  syphi- 
litic infection,  had  caused  haemorrhage,  or  an  outbreak  of  localized 
syphilitic  inflammation  in  the  spinal  canal  in  a  way  to  exert  pres- 


174 


ORGANIC   EFFECTS   OF   INJURY. 


sure  upon  the  spinal  cord.  From  this  condition  the  patient  appar- 
ently recovered.  There  was  left,  however,  a  locus  minoris  resisten- 
ticE,  as  was  shown  by  the  progressive  muscular  atrophy  first  ap- 
pearing in  the  muscles  which  had  previously  been  the  seat  of  the 
-temporary  paralysis. 

The  following  case,  which  has  been  under  our  observa- 
tion at  the  clinic  for  many  months,  developed  progressive 
muscular  atrophy  three  months  after  a  blow  on  the  back : 


Fig.  38. — Case  of  progressive  muscular  atrophy  which  began  three  months  after  an 
injury  to  the  back.  The  photograph  shows  the  wasting  of  the  shoulder  and 
chest  muscles  and  the  7nain  e7i  griffe.     ( Vanderbilt  Clinic. ) 


The  patient  (Figs.  38  and  39)  says  that,  as  far  as  he  knows, 
there  have  never  been  any  nervous  diseases  in  his  family,  and  that 
previous  to  his  present  illness  he  himself  had  always  been  strong 
and  well.    As  a  young  man  he  had  gonorrhoea,  but  denies  all  symp- 


PROGRESSIVE    MUSCULAR   ATROPHY.  175 

toms  of  syphilis.     He  was  married  at  twenty-nine  years  of  age, 
and  has  one  healthy  child.     His  wife  never  had  any  miscarriages. 


Fig.  39. — Same  patient  as  in  Fig.  38,  showing  wasting  of  back  muscles. 

He  is  a  moderate  drinker.  At  the  age  of  thirty-one,  eight  years 
ago,  the  patient  weighed  one  hundred  and  seventy-five  pounds, 
and  was  healthy  and  strong.     As  the  proprietor  of  a  rag  shop  he 


1^6  ORGANIC  EFFECTS  OF  INJURY. 

was  daily  engaged  in  handling  heavy  packages,  an  exercise  which 
he  could  perform  without  unusual  effort  or  fatigue.  The  man  is 
intelligent  and  straightforward,  has  no  object  to  deceive,  and  every 
statement  he  makes  relative  to  his  physical  condition  previous  to 
the  accident  indicates  that  he  was  a  healthy,  active,  muscular  man. 

In  1889 — that  is,  about  eight  years  ago — while  lifting  one  end 
of  a  bale  of  cotton,  weighing  eight  hundred  pounds,  he  slipped  and 
fell  so  that  one  corner  of  the  bale  struck  him  in  the  small  of  the 
back.  He  suffered  no  pain,  and  was  able  to  get  up  and  return  to 
work,  and  for  three  months  observed  no  ill  effects  from  the  acci- 
dent. Then  he  began  to  have  pain  in  the  small  of  the  back  and 
in  the  muscles  of  the  right  arm,  with  some  loss  of  power,  espe- 
cially for  movements  of  extension  of  the  wrist  and  of  the  fingers. 
The  weakness  of  the  right  upper  extremity  soon  became  so  marked 
that  he  had  to  give  up  working  with  it.  One  year  after  the  acci- 
dent the  left  hand  and  arm  became  similarly  affected.  At  this 
time  he  also  noticed  the  hands  were  becoming  very  much  thinner 
between  the  thumbs  and  fingers,  and  that  there  was  a  decided 
sinking  in  around  the  thumbs.  The  fingers  became  stiff,  which 
was  observed  particularly  upon  attempts  to  extend  them.  He  soon 
became  so  incapacitated  that  he  was  obliged  to  give  up  all  heavy 
work.  With  the  exception  of  slight  pain,  there  were  never  any 
sensory  disturbances,  and  the  functions  of  the  bladder  and  rectum 
remained  normal. 

The  condition  of  wasting  has  been  progressive,  and  to-day  the 
man  presents  a  picture  of  progressive  muscular  atrophy,  type 
Duchenne-Aran,  with  beginning  involvement  of  the  leg.  There  is 
extensive  atrophy  of  the  thenar  and  hypothenar  eminences  and  of 
the  interosseous  muscles.  Both  hands  are  in  the  attitude  of  main 
en  griff e.  The  dorsal  surface  of  the  thumb  is  in  the  same  plane  as 
the  back  of  the  fingers,  and  its  opposability  is  lost.  There  is  also 
an  atrophy  of  the  flexors  and  extensors  of  the  wrists,  the  deltoids, 
the  pectoral  muscles,  and  the  muscles  of  the  back,  especially  of 
the  right  side.  There  is  also  a  beginning  atrophy  of  the  left  an- 
terior tibial  muscles,  so  that  the  patient  has  the  "stepping"  or 
"equine"  gait  on  that  side.  The  atrophied  muscles  are  the  seat 
of  fibrillary  twitchings,  which  become  very  marked  on  exertion. 
All  the  muscles,  with  the  exception  of  those  which  are  wholly 
atrophied — as  are  some  of  the  interossei — and  of  the  ones  which 
are  held  stiff  by  contractures,  react  readily  to  faradism.  The  knee- 
jerks  are  present,  and  there  are  no  sensory  disturbances.  The 
patient  is  practically  deprived  of  all  use   of  the  upper  extremities. 


PROGRESSIVE    MUSCULAR   ATROPHY.  177 

The  paralysis  and  deformities  of  the  fingers  and  hands  prevent 
any  fine  co-ordinated  movements,  and,  on  account  of  the  loss  of 
power  in  the  shoulder  muscles,  he  can  with  difficulty  lift  his  hands 
to  his  head,  or  hold  his  arms  out  from  his  body.  As  a  conse- 
quence he  can  do  no  manual  work,  can  not  dress  himself,  and  can 
only  with  difficulty  feed  himself.  His  condition  is  slowly  but 
steadily  becoming  worse,  and  has  recently  become  complicated  by 
tubercular  disease  of  the  right  lung. 

The  only  medico-legal  question  which  might  arise  in  regard  to 
this  case  is  whether  the  condition  is  solely  due  to  the  injury. 
There  can  be  no  doubt  as  to  the  correctness  of  the  diagnosis; 
every  symptom  is  present,  and  the  patient  presents  a  typical  pic- 
ture of  the  Duchenne-Aran  type.  The  symptoms  appeared  a  short 
time  after  injury  in  a  man  who  had  undoubtedly  been  strong  and 
well  before,  and  who  was  in  no  way  predisposed  to  disease.  The 
injury  was  sufficiently  severe  to  cause  considerable  violence  to 
the  back,  and  it  seems  to  me  entirely  reasonable  to  believe  that 
had  it  not  been  received  the  spinal  disease  would  not  have  devel- 
oped. 

Bibliography. 

Ballet  and  Dutil.     Reime  de  medicine,  January,  1884. 

Bullard,  A  Case  of  Progressive  Muscular  Atrophy  following  a 
Blow  on  the  Head.     Boston  Med.  and  Snrg.  Jour.,  1885,  p.  369. 

Charcot,  J.  B.,  Contribution  a  I'etude  de  I'atrophie  muse,  prog., 
Paris,  1895. 

Clarke  and  Jackson,  On  a  Case  of  Muscular  Atrophy,  with  Dis- 
ease of  the  Spinal  Cord  and  Medulla  Oblongata.  Medico-Chirurg. 
Tratis.,  1867,  vol.  1,  p.  489. 

Eisenlohr,  Klinische  und  Anatomische  Beitrage  zur  progressive 
Bulbarparalyse.     Zeit.  fiir  klin.  Med.,  1880,  vol.  i,  3,  p.  435- 

Hirsch,  Amyotrophic  Lateral  Sclerosis  following  Old  Polio- 
myelitis.    Med.  News.,  1895,  vol.  Ixvii,  p.  500. 

Mann,  A  Case  of  Traumatic  Progressive  Muscular  Atrophy  of 
Long  Duration,  complicated  by  an  Attack  of  Left  Hemiplegia,  due 
to  Embolism.     Alienist  and  Neurologist,  1886,  vol.  vii,  p.  430. 

Raymond,  Atrophies  musculaires,  Paris,  1889,  p.  138. 

Ziehen,  Aerztliches  Gutachten  uber  einen  forensischen  Fall 
von  progressiven  Muskelatrophie.  Viertjahrs.  fur  gerich.  Med., 
1894,  vol.  viii,  p.  286. 


1^8  ORGANIC  EFFECTS  OF  INJURY. 


Paralysis     Agitans     (Parkinson's     Disease — Shaking 

Palsy). 

Examination  of  the  properly  prepared  brain  and  spinal 
cord  of  a  person  dead  with  paralysis  agitans  shows  degen- 
erations in  nerve  fibers  and  nerve  cells  and  in  connective 
tissue.  Since,  however,  disease  occurs  almost  altogether  in 
persons  who  have  reached  the  age  when  such  degenerations 
often  occur  without  causing  the  symptoms  of  any  distinct 
disease,  it  still  remains  to  be  proved  whether,  in  paralysis 
agitans,  the  anatomical  alterations  are  causes  or  effects,  or 
simply  accompaniments  of  the  malady.  But,  although  the 
pathology  remains  unexplained,  the  fact  that  in  it  the  central 
nervous  system  appears  differentlv  than  in  health,  together 
with  the  fact  that  the  clinical  manifestations  indicate  the 
action  of  a  common  structural  cause,  are  sufficient  to  permit 
the  disease  to  be  classified  without  impropriety  among  the 
organic  nervous  diseases. 

The  symptoms  which  are  the  most  constant,  and  which 
give  the  disease  its  clinical  characters,  are  tremor,  rigidity, 
and  weakness.  The  tremor  is  rhythmical  and  comparatively 
coarse,  there  being  between  five  and  seven  excursions  in  a 
second.  It  continues  during  rest,  ceases  during  sleep,  and 
although  not  at  all  or  only  slightly  aggravated  in  intended 
movements,  it  is  made  very  much  worse  by  emotional  influ- 
ences. The  tremor  usually  originates  in  the  thumb  and  in- 
dex finger  of  one  hand,  and  from  there  it  spreads  to  other 
fingers.  Later  it  involves  the  wrist  and  the  muscles  of  the 
whole  upper  extremity.  i\fter  it  has  persisted  for  a  longer 
or  shorter  time  in  any  one  part,  its  usual  course  is  that  of 
extension.  The  mode  of  extension,  which  is  fairly  though 
not  absolutely  constant,  is  from  the  arm  to  the  leg  on  the 
same  side,  and  then  to  the  arm  and  the  leg  on  the  opposite 
side.     In  the  rare  cases  in  which  the  tremor  begins  in  the 


PARALYSIS   AGITANS. 


179 


leg,  it  may  follow  the  hemiplegic  type,  or  it  may  involve  the 
opposite  leg,  before  passing  up  to  the  arm. 

The  head  and  shoulder  muscles  are  rarely  involved  ;  these 
parts  are  caused  to  oscillate  by  the  transmitted  movements 
from  the  limbs,  but  it  is  only  in  very  exceptional  cases  that 
they  are  themselves  the  seat  of  tremor. 

Muscular  rigidity  and  weakness  are  symptoms  of  equal 
importance  to  the  tremor,  and  occasionally  cases  are  met 
with  in  which  they  are  present  without  the  tremor,  furnish- 
ing the  seeming  paradox  of  paralysis  agitans  without  agi- 
tation. 

In  the  larger  number  of  cases,  however,  the  rigidity  and 
weakness  develop  in  the  same  parts  and  at  the  same  time  as 
the  tremor.  The  rigidity  consists  in  a  stiffness  of  the  mus- 
cles without  increase  of  the  refilexes,  and  is  consequently 
different  from  spasticity  ;  it  can  usually  be  overcome  with- 
out difficulty  by  the  physician.  The  loss  of  power  is  never 
absolute,  but  all  the  movements  of  the  affected  muscles 
are  slow  and  uncertain. 

When  the  disease  is  well  developed  the  muscular  condi- 
tions give  rise  to  characteristic  appearances.  The  face  (Fig. 
40)  is  expressionless  and  drawn.  The  eyes  are  wide  open, 
and  there  is  very  little  play  of  the  features  in  talking  or  in 
emotional  expressions.  The  voice,  from  stiffness  of  the 
muscles  of  the  larynx,  changes  its  pitch  but  little  and  is 
monotonous.  The  head  is  bent  forward  (Fig.  41),  and  there 
is  frequently  a  bending  forward  of  the  spine.  The  limbs  are 
flexed  at  the  large  joints  ;  the  fingers  are  fiexed  at  the  first 
phalanges,  and  extended  at  the  second  and  third  (interosseous 
position).  The  gait  is  shuffling,  the  patient  walking  with 
short  steps,  and  having  difficulty  in  starting,  or,  having  once 
started,  in  stopping  himself.  Festination,  or  the  tendency  to 
constantly  increase  the  rapidity  of  the  gait,  and  retropulsion 
and  propulsion,  or  the  tendency  to  fall  backward  or  forward, 
as  the  result  of  slight  pushes,  are  common  symptoms.    There 


i8o 


ORGANIC  EFFECTS  OF  INJURY. 


are  no  chang-es  in  reflex  action,  no  atrophy  or  disturbances 
of  sphincter  action.  Cutaneous  sensibility  remains  normal, 
although  the  patients  frequently  complain  of  subjective  dis- 
turbances of  sensation.  The  disease  follows  a  chronic  and 
progressive  course,  and  is  incurable,  although  it  may  last  for 


Fig.  40. — Showing  facial  expression  and  position  of  the  hands  in  paralysis  agitans.  . 
(Incurable  Hospital.) 

an  indefinite  number  of  years.  The  symptoms  have  been  de- 
scribed in  some  detail,  because  the  order  of  their  develop- 
ment after  injury  is  our  chief  proof  of  the  traumatic  astiology 
of  the  disease. 

iEtiology. — There  are  few  disorders  of  the  nervous  sys- 


PARALYSIS   AGITANS. 


I8l 


tem  in  which  predisposition  is  so  seldom  demonstrable  as  in 
paralysis  agitans.  In  a  small  proportion  of  the  cases  the 
disease  itself,  or  epilepsy,  or  insanity,  may  be  shown  to  have 
existed  in  relatives,  but  gen- 
erally persons  who  become 
the  subjects  of  Parkinson's 
disease  have  healthy  ances- 
tors, and  have  themselves 
been  previously  healthy.  The 
disease  occurs  most  common- 
ly in  the  decades  of  life  be- 
tween forty  and  sixty,  and  is 
more  frequent  in  men  than  in 
women  (five  to  three).  Ac- 
cording to  Gowers,  exciting 
causes  can  be  found  in  one 
third  of  the  cases,  of  which 
the  only  ones  requiring  de- 
scription here  are  nervous 
shock  and  physical  injury. 

Gowers  believes  fright  to 
be  the  essential  feature  in  the 
genesis  of  this  disease. 

In  support  of  this  view  he 
cites  the  case  of  a  man  who  was 
waked  by  a  bell  on  account  of  a 
fire  ;  for  a  year  and  a  half  the 
same  bell  always  caused  tran- 
sient tremor,  which  then  became 
permanent,  and  passed  into  the 
typical  form  of  paralysis  agitans. 

Also,  the  case  of  a  woman 
who,  at  thirty -seven  years  of 
age,  was  sitting  quietly  at  work, 
when  a  stream  of  water  sudden- 
ly flowed  from  a  tap  onto  her  left  wrist.  She  was  much  startled  ; 
the  left  arm  immediately  began  to  shake,  and  the  tremor  per- 
13 


Fig.  41.  — Showing  characteristic  atti- 
tude in  paralysis  agitans.  (Vander- 
bilt  Clinic.) 


l82  ORGANIC    EFFECTS   OF    INJURY. 

sisted,  passing  to  the  leg,  and   afterward  to   the  limbs  on  the  left 
side. 

That  the  disease  often  appears  and  becomes  permanent 
soon  after  a  severe  shock,  without  any  physical  injury,  there 
can  be  no  doubt,  but  more  frequently  there  has  been  phys- 
ical injury  as  well.  Of  one  hundred  and  thirty-nine  cases 
observed  at  the  Vanderbilt  clinic,  fright  is  assigned  as  the 
sole  cause  in  seven.  On  the  other  hand,  of  twenty-six  trau- 
matic cases  examined  by  Walz,  there  is  no  mention  of  fright 
alone  as  a  cause,  when  unaccompanied  by  physical  injury. 

The  injury,  which  is  usually  moderately  severe,  may  be 
of  different  kinds.  Paralysis  agitans  has  immediately  devel- 
oped after  falls,  injuries  to  nerves,  stab  wounds,  contusions^ 
fractures,  etc.  Walz's  analysis  showed,  in  twenty  six  cases, 
general  concussion,  six ;  wounds  (stabs  and  cuts),  seven ; 
burning  and  freezing,  one ;  sprains,  twists,  and  fractures, 
four;  contusions,  eight. 

Some  connection  between  the  part  injured  and  the  local- 
ity of  the  earliest  symptoms  is  almost  unexceptional.  If  the 
injury  were  limited  to  one  hand,  the  tremor  and  stiffness  be- 
gin in  that  hand  ;  if  there  were  fractures  of  bone,  or  contu- 
sions or  injuries  to  nerves  of  one  extremity,  the  symptoms 
first  appear  in  that  extremity. 

Thus  a  male  patient,  aged  sixty,  at  the  Vanderbilt  clinic,  was 
in  a  runaway  accident  and  was  thrown  out,  striking  the  left  arm 
and  shoulder.  Tremor  began  soon  after  in  the  left  arm,  and 
eventually  extended  to  the  leg. 

Such  a  relationship  might  be  regarded  as  coincidental  if 
it  were  true  only  of  the  upper  extremity,  where  the  disease 
regularly  begins ;  but  it  is  also  almost  always  true  for  those 
other  parts  in  which  non-traumatic  paralysis  agitans  only- 
very  exceptionally  has  its  initial  symptom. 

Charcot  reports  two  cases  in  which  the  influence  of  the 
injury  upon  the  development  of  symptoms  appears  unques- 
tionable.    In  one — 


PARALYSIS   AGITANS.  1 83 

A  woman  fell  out  of  a  wagon  and  received  a  contusion  of  the 
left  side.  She  soon  had  severe  pain,  referred  to  the  sciatic  nerve, 
and  in  a  short  time  the  whole  limb  began  to  shake.  The  tremor 
was  permanent,  and  extended  to  all  the  other  members. 

In  the  other  case  a  woman  suffered  a  dislocation  of  the  jaw. 
The  paralysis  agitans,  which  soon  developed  and  eventually  be- 
came general,  first  appeared  in  the  jaw. 

When  the  injury  is  general,  such  as  a  concussion  of  the 
whole  body,  the  symptoms  begin  in  one  or  both  of  the  up- 
per extremities,  thus  acting  similarly  to  progressive  muscu- 
lar atrophy  when  it  occurs  in  those  parts  which  had  previ- 
ously been  affected  through  spinal  injury. 

Thus  in  a  case  described  by  Walz : 

Male,  aged  sixty-one  years,  laborer.  No  syphilis  or  alcoholism. 
Heredity  negative.  Was  struck  on  the  back  of  the  head  by  a 
package  weighing  about  sixty-five  pounds,  which  had  fallen  from 
a  fifth-story  window.  The  patient  was  knocked  down  and  ren- 
dered momentarily  unconscious.  After  ten  minutes  he  got  up 
and  walked  home.  For  two  weeks  he  was  in  bed,  with  pains  in 
the  upper  extremity  from  the  neck  to  the  fingers,  with  rhythmical 
movements  of  both  hands  and  of  the  head.  The  patient  recov- 
ered sufficiently  to  get  up,  but  he  could  not  work,  and  he  was 
granted  a  pension,  in  accordance  with  the  German  law,  for  "  pa- 
ralysis agitans,  which  was  the  direct  result  of  injury."  The  patient 
died  from  spasm  of  the  respiratory  muscles  four  years  after  the 
accident.  The  autopsy  report  says:  "There  are  no  local  findings, 
and  certainly  no  haemorrhages  of  old  or  recent  date.  No  marked 
atheroma,  and  nothing  abnormal  in  the  dura  or  bones." 

Paralysis  agitans  often  develops  at  the  site  of  an  injury 
received  years  before.     Examples  of  this  are  very  common : 

A  patient  of  mine,  when  a  young  man,  received  a  severe  mu- 
tilation of  the  right  hand.  The  wound  healed  perfectly,  and 
although  the  right  hand  remained  practically  useless,  the  patient 
for  twenty  years  had  no  symptoms  of  nervous  disease.  At  the 
end  of  that  time  the  right  wrist  and  arm  began  to  shake,  and  gen- 
eral paralysis  agitans  eventually  developed.  From  the  Vanderbilt 
clinic  records  may  be  quoted  the  case  of  a  man  who,  at  the  age  of 
forty,  cut  the  ulnar  side  of  his  right  wrist.     Paralysis  agitans  ap- 


l84  ORGANIC  EFFECTS  OF  INJURY. 

peared  twenty-two  years  later ;  it  began  in  tlie  right  hand.  Also 
that  of  a  man,  three  fingers  of  whose  left  hand  were  amputated 
at  the  age  of  thirty,  and  in  whom  the  first  symptom  of  paralysis 
agitans,  coming  on  at  the  age  of  sixty-three,  consisted  of  tremor 
in  the  operated  hand. 

In  such  cases,  on  account  of  the  long-time  interval,  the 
injury  can  only  be  regarded  as  a  predisposing  cause. 

TJie  intermediate  or  the  "'bridge''  symptoms,  which  exist 
between  the  receipt  of  the  injury  and  the  appearance  of  the 
symptoms  of  paralysis  agitans,  consist  in  general  nervous 
shock  and  in  pain,  weakness,  and  some  stiffness  in  the  parts 
which  are  to  become  the  seat  of  the  tremor. 

They  usually  appear  soon  after  the  injury.  To  refer 
once  more  to  Walz's  analysis,  tremor  appeared  at  once,  or 
within  a  day,  in  eight ;  soon,  or  in  a  few  days  in  seven  ;  after 
one  to  eight  months,  in  seven ;  and  after  one  to  four  years, 
in  four. 

The  tremor  is  the  first  pronounced  symptom  to  appear  ; 
the  other  symptoms  are  of  gradual  development  and  do  not 
vary  essentially  in  their  course  from  the  symptoms  of  the 
disease  when  it  occurs  independently  of  traumatic  influ- 
ences. 

It  is  impossible  to  explain  the  genesis  of  traumatic  paraly- 
sis agitans  further  than  to  note  the  sequence  of  events  and 
to  infer  that  the  injury  stands  in  some  causal  relation  to  the 
disease.  Walz  believes  that  the  disease  can  only  appear  in 
persons  whose  nervous  systems  are  already  deteriorated. 
While  the  truth  of  such  a  theory  can  not  be  denied,  it  can 
not  be  proved,  because  it  is  rarely  possible  to  demonstrate 
any  predisposition  in  the  patient. 

While  it  may  seem  reasonable  to  suppose,  at  least  after 
slight  injuries,  that  the  disease  would  have  eventually  devel- 
oped under  any  circumstances,  there  are  no  means  of  know- 
ing that  such  would  have  been  the  case. 


PARALYSIS   AGITANS. 


Bibliography. 


185 


Charcot,  Qiiuvres  completes.     Paris,  1891,  i,  p.  155. 

Vandier,  De  la  paralysie  agitante  de  cause  traumatique.  These 
de  Paris,  1886. 

Walz,  Die  traumatische  Paralysis  Agitans.  Vierteljahrs.  f. 
gerich.  Med.,  1896,  xii,  p.  323. 

Gowers,  Diseases  of  the  Nervous  System.     London,  1893. 


PART    IL 

FUNCTIONAL  EFFECTS  OF  INJURY— THE  NERV- 
OUS DISORDERS  WHICH  MOST  FREQUENTLY 
FOLLOW  RAILWA  Y  AND  ALLIED  ACCIDENTS— 
THE    TRAUMATIC  NEUROSES. 

CHAPTER   I. 

INTRODUCTORY  CONSIDERATIONS  REGARDING  THE  HISTORY, 
NOMENCLATURE,  PATHOLOGY,  CAUSATION,  AND  SYMP- 
TOMS  OF   THE   TRAUMATIC   NEUROSES. 

An  eventful  pathological  history  attaches  to  those  nerv- 
ous disorders  which  most  frequently  follow  railway  and 
allied  accidents  and  in  which  there  is  no  reason  to  suppose 
that  there  have  been  gross  lesions  to  the  nervous  system. 
Explained  at  first  on  a  theory  of  disturbance  of  vascularity 
of  the  spinal  cord,  they  were  later  thought  to  depend  upon 
multiple  areas  of  inflammation  disseminated  throughout  the 
whole  cerebro-spinal  axis.  They  have  been  successively  re- 
garded as  nearly  altogether  organic,  nearly  altogether  func- 
tional, or  nearly  altogether  feigned.  They  have  been  named 
after  two  men — Erichsen  and  Oppenheim — who  held  very 
different  views  as  to  their  nature.  They  have  been,  and  still 
are,  called  by  many  different  titles,  chief  of  which  are  rail- 
way spine,  railway  brain,  concussion  of  the  spinal  cord, 
concussion  of  the  brain,  spinal  anaemia,  spinal  irritation, 
traumatic  neurosis,  traumatic  h37steria,  traumatic  neurasthe- 
nia, and  traumatic  hystero-neurasthenia.  These  disorders 
have  become  uninterruptedly  more  frequent  and  more  im- 
portant.    They  are  accident  neuroses,  and  we  live  in  an  age 


HISTORY   OF   THE    TRAUMATIC   NEUROSES.  187 

of  accidents  ;  they  often  result  from  actionable  negligence, 
and  the  frequency  of  actions  brought  for  personal  injuries  is 
constantly  increasing.  More  intimate  familiarity  with  the 
general  diseases  of  the  nervous  system  has  perfected  our 
powers  in  the  diagnosis  of  all  nervous  affections,  and  it  now 
seems  that  most  of  these  functional  traumatic  neuroses  can 
be  properly  classified,  even  though  they  may  not  be  per- 
fectly understood. 

Such  a  classification  and  description  will  be  the  object  of 
the  following  pages,  and  may  be  best  accomplished  by  first 
passing  in  review  the  various  opinions  of  men  who  have 
contributed  to  this  subject. 

Although  concussion  of  the  spine  had  been  described  by 
Abercrombie,  Ollivier,  and  others,  the  first  important  writer 
on  railway  injuries  was  Erichsen.     Erichsen  was  a  surgeon, 
and  wrote  at  a  time  when  nervous  disease  was  but  little  un- 
derstood.    Gross  lesions,   such   as  haemorrhage   and    acute 
softening,  were   of   course   recognized,   but  almost  nothing 
was  known  of  the  microscopical  pathology  of  the  nervous 
system.     Had   Erichsen  been  the  most  expert  neurologist 
of  his  time  he  could  have  known  the  finer  anatomy  of  none 
of  the  degenerative  diseases  except  locomotor  ataxia.     The 
knowledge  of  nervous  symptomatology  was  corresponding- 
ly imperfect.     From  Erichsen's  descriptions  it  is  very  hard 
to  tell  what  many  of  his  patients  suffered   from.     He  evi- 
dently did  not  recognize  the  differences  between  ataxia  and 
paralysis,  for  in  the  case  of  posterior  spinal  degeneration, 
which  will  be  referred  to  later,  he  describes  the  symptoms 
as  paralytic  when  in  reality  they  were  ataxic.     He  says  little 
about   electrical  reactions,   does  not  examine  the    reflexes, 
and  makes  very  cursory  mention  of  anissthesia.     Erichsen 
(I  quote  from  the  later  edition  of  his  book)  recognized  that 
these  disorders  were  not  necessarily  the  exclusive  results  of 
railway  accidents. 

Of  his  fifty-three  cases  only  seventeen  were  injured  on 


1 38  FUNCTIONAL  EFFECTS  OF  INJURY. 

railways.  In  most  of  the  others  the  violence  acted  immedi- 
ately on  the  spine,  as  in  direct  blows,  injury  to  the  back  by 
the  falling  of  trees,  etc.,  or  in  falls  from  considerable  heights 
on  the  head  or  on  the  buttocks. 

The  violence  was  generally  severe,  and  entirely  capable 
of  fracturing  bone  or  rupturing  ligaments,  and  not  the  kind 
of  violence  which  is  most  frequently  associated  with  railway 
injuries.  Many  of  his  cases  give  evidence  of  severe  organic 
lesion  of  the  nervous  system,  and  would  to-day  undoubtedly 
be  regarded  as  depending  upon  visible  anatomical  changes 
of  a  morbid  character.  They  would  now  be  explained,  not 
as  Erichsen  explained  them,  by  an  assumption  of  molecular 
changes  in  the  spinal  cord,  but  by  the  occurrence  of  such 
visible  damage  as  may  be  caused  by  compression  of  nervous 
tissue  from  splinters  of  bone  or  by  haemorrhages  resulting 
from  laceration  of  blood-vessels,  or  from  the  wounding  of 
any  of  the  intraspinal  structures.  Of  only  a  few  of  Erich- 
sen's  cases  can  it  be  said  with  reasonable  certainty  that  they 
were  functional — not  dependent  upon  local  conditions  of  an 
organic  character,  but  due  to  a  functional  disorder  of  the 
whole  nervous  system.  These  latter  Erichsen  did  not  rec- 
ognize for  what  they  really  were. 

With  the  exception  of  one  case  of  syphilis  of  the  nervous 
system  he  apparently  did  not  appreciate  the  possible  influ- 
ence of  trauma  upon  hastening  the  clinical  manifestations  of 
latent  nervous  disease.  He  also  failed  to  distinguish  be- 
tween symptoms  of  spinal  and  cerebral  origin.  For  exam- 
ple, he  reports  a  case  (No.  48)  of  paraplegia,  with  involve- 
ment of  the  face,  as  due  to  spinal  injur3^ 

Confusion  will  invariably  result  in  the  mind  of  any  one 
who  begins  the  study  of  traumatic  nervous  disease  by  a 
perusal  of  Erichsen's  work.  He  will  there  find  grouped  to- 
gether cases  which  are  evidently  of  very  diverse  character. 
Erichsen  makes  of  concussion  both  a  cause  and  an  effect. 
For  him,  concussion  is  not  only  the  shock,  the  jar  of  the 


HISTORY    OF    THE    TRAUMATIC    NEUROSES. 


189 


accident,  but  it  is  also  the  disarrangement  of  molecular 
structure  of  the  spinal  cord  which  may  result  in  alterations 
of  blood  supply  (anaemia — hyperasmia)  sufficient  to  give 
clinical  symptoms. 

Erichsen's  theory  of  concussion  of  the  spinal  cord  as  a 
pathological  entity  was  purely  hypothetical.  Microscopical 
.technique  is  more  advanced  now  than  it  was  at  the  time  he 
wrote,  yet  it  has  thus  far  failed  to  disclose  not  only  molecu- 
lar pathology,  but  any  such  thing  as  molecular  structure. 
Molecular  disorders  are  still  in  the  domain  of  speculative 
science.  The  significance  of  local  spinal  anaemia  and  hyper- 
semia,  to  which  he  ascribed  much  importance  is  absolutely 
unknown.  It  is  not  intended  to  cast  any  discredit  upon 
Erichsen  or  his  work,  but,  writing  at  the  time  he  did,  it 
would  have  been  impossible  for  him  to  formulate  a  theory 
which  could  serve  as  an  authority  to-day.  The  following 
case,  his  one  autopsy  for  the  determination  of  the  pathology 
of  spinal  concussion,  seems  to  prove  this: 

Patient,  fifty-two  years  of  age  at  the  time  of  his  death,  a  man 
of  active  business  habits,  had  been  in  a  railway  collision.  Imme- 
diately after  the  collision  the  patient  walked  from  the  train  to 
the  station,  which  was  close  at  hand.  He  had  received  no  external 
sign  of  injury,  no  contusions  or  wounds,  but  he  complained  of  a 
pain  in  his  back.  Being  most  unwilling  to  give  in,  he  made  every 
effort  to  get  about  in  his  business,  and  did  so  for  a  short  time 
after  the  accident,  though  with  much  distress.  Numbness  and  a 
want  of  power  in  the  muscles  of  the  lower  limbs  gradually  but 
steadily  increasing,  he  soon  became  disabled.  His  gait  became  un- 
steady, /zke  t/ia^  0/  a  /ta/f-in^oxica^ed  J>erson.  ...  In  the  latter  part 
of  his  illness  some  weakness  of  the  upper  extremities  became  appar- 
ent, so  that,  if  the  patient  were  off  his  guard,  a  cup  or  a  glass  would 
slip  from  his  fingers.  .  .  .  There  was  no  paralysis  of  the  sphincter 
of  the  bladder  until  about  eighteen  months  before  his  death. 

This  is  apparently  the  description  of  a  case  of  locomotor 
ataxia,  and  the  autopsy  by  Lockhart  Clarke,  instead  of  fur- 
nishing an  explanation  of  the  pathology  of  spinal  concussion, 
as   Erichsen  supposed  it  did,  added  one  more  to  the  list,  at 


ipO  FUNCTIONAL   EFFECTS   OF   INJURY. 

that  time  small,  of  the  recorded  cases  of  primary  degenera- 
tion of  the  posterior  columns  of  the  spinal  cord.  Dr.  Clarke 
says  in  his  autopsy  report : 

The  membranes  at  some  parts  were  thickened,  and  adherent  at 
others,  to  the  surface  of  the  white  columns.  .  .  .  On  making  sec- 
tions ...  of  all  the  white  columns,  the  posterior  were  exclusively 
the  seat  of  the  disease.  These  columns  were  darker,  browner, 
denser,  and  more  opaque  than  the  antero-lateral,  and  in  their 
preparations  under  the  microscope  this  appearance  was  found  to 
be  due  to  a  multitude  of  granular  corpuscles  and  isolated  granules 
and  to  an  exuberance  of  wavy  fibrous  tissue  disposed  in  a  longi- 
tudinal direction. 

Erichsen  did  not  appreciate  that  many  serious  disturb- 
ances of  general  nervous  function  may  result  from  injury 
and  shock  when  there  has  been  no  local  damage  to  the  nerv- 
ous system  itself. 

Thus,  Case  6,  which  he  describes  as  "  concussion  from 
a  fall  out  of  a  bathing  machine,"  might  be  construed  as  a 
case  of  hysterical  paraplegia,  or  of  astasia-abasia : 

A  young  lad,  fourteen  years  old,  fell  in  shallow  water,  striking 
the  sandy  bottom.  He  received  no  mark  of  external  injury  and 
walked  home.  His  legs  gradually  became  weak  and  numb. 
Erichsen  found,  ten  days  later,  that  "  he  was  quite  unable  to  stand, 
but  when  lying  in  bed  could  kick  out  his  legs  quite  in  a  natural 
way."     He  recovered  completely  in  four  months. 

Erichsen's  work,  however,  possesses  more  than  a  merely 
historical  value.  It  called  attention  to  the  possibility  of 
fractures  of  vertebrae  and  of  tearing  of  ligaments  without 
external  evidences  of  injury,  and  proved  that  serious  nerv- 
ous symptoms  may  result  from  injuries  which  at  first  appear 
trivial.  But  he  left  almost  untouched  the  complicated  ques- 
tions involved  in  the  greater  number  of  railway  injuries,  and, 
through  a  failure  to  recognize  the  frequent  subjective  char- 
acter of  the  symptoms,  his  work  is  to  be  regarded  as  a  con- 
tribution to  surgery  rather  than  to  neurology.  It  remained 
for  subsequent  writers,  more  experienced  than  he  in  general 


HISTORY   OF   THE    TRAUMATIC   NEUROSES.  191 

nervous  diseases,  as  well  as  in  the  forms  which  most  fre- 
quently result  from  railway  accidents,  to  explain  the  chain 
of  symptoms  which  are  most  commonly  recited  by  injured 
persons  to  claim  agents,  and  which  are  now  called  the  neu- 
roses of  traumatic  origin. 

While  Erichsen's  book  marks  the  beginning  of  the  study 
of  the  nervous  disorders  following  railway  and  allied  in- 
juries, it  was  a  long  time  before  their  true  nature  was  un- 
derstood. Ten  years  after  Erichsen's  first  edition,  Erb  still 
believed  in  molecular  disturbance  as  the  chief  element  of 
concussion.  Westphal,  in  1878,  reports  three  cases,  in  two 
of  which  the  symptoms  were  so  widely  disseminated  and  so 
pronounced  that  he  ascribed  them  to  multiple  areas  of  cere- 
bro-spinal  softening. 

Rigler,  in  1879,  thought  that  in  many  cases  the  symptoms 
were  exaggerated  or  assumed.  In  the  absence  of  exaggera- 
tion or  feigning,  he  regarded  the  symptoms  as  due  to  or- 
ganic lesions. 

In  America,  Hodges  was  the  first  to  object  to  Erichsen's 
pathological  views.  In  1880  he  read  a  paper  before  the 
Boston  Society  for  Medical  Improvement,  in  which  he  said 
that  "  we  have  no  knowledge  to  justify  the  proposition  that 
what  is  popularly  called  '  concussion  of  the  spine  '  is  due  to 
a  molecular  disarrangement  of  the  cord  by  an  assumed  shake 
or  jar.  That  vascular  disturbances  (anaemia,  hypersemia, 
haemorrhages,  spinal  apoplexy)  followed  by  meningitis,  mye- 
litis, or  degenerative  changes  of  the  spinal  cord,  are  shown 
by  experimental  pathology,  and  to  a  certain  extent  by  post- 
mortem examinations,  to  be  the  true  cause  of  symptoms 
heretofore  commonly  designated  as  concussion  of  the  spine." 
He  thought  Erichsen's  book  "  presents  an  exaggerated  pic- 
ture of  its  symptoms  and  consequences  which  are  not  justi- 
fied by  our  present  knowledge  of  the  subject."  Hodges 
also  suggested  the  possible  functional  character  of  many  of 
the  symptoms. 


IQ2  FUNCTIONAL   EFFECTS   OF    INJURY. 

It  remained,  however,  for  Page  to  prove,  as  conclusively 
as  such  things  can  be  proved,  that  although  falls,  jars,  and 
shocks  might  cause  organic  injury  to  the  spinal  cord,  such 
a  result  is  relatively  infrequent;  that  railway  accidents,  in 
which  the  factors  of  concussion  and  fright  are  so  intimately 
mingled,  more  frequently  caused  nervous  disorders  of  a 
functional  than  of  an  organic  character.  Page  was  surgeon 
to  the  London  and  Northwestern  Railway  of  England,  and 
had  had  a  very  large  experience  in  railway  cases.  His  ex- 
perience was  essentially  different  from  Erichsen's,  in  that, 
as  a  corporation  surgeon,  he  saw  man}^  cases  of  trifling  in- 
jury, and  had  to  be  constantly  on  his  guard  against  impos- 
ture and  exaggeration.  His  work  bears  the  marks  of  in- 
telligent and  impartial  observation,  and  although  he  may 
have  been  to  a  certain  extent  prejudiced  in  favor  of  the  rail- 
way, many  of  his  views  have  been  substantiated  by  subse- 
quent observers.  Page  saw  the  errors  of  Erichsen's  work, 
and  emphasized  the  important  fact  that  there  had  been  no 
satisfactory  pathological  proof  of  disease  of  the  spinal  cord 
resulting  from  concussion,  as  distinguished  from  recogniza- 
ble injury.  He  showed  that  the  discussions  regarding  spinal 
concussion  were  entirely  empirical,  and  that  there  was  no 
proof  to  show  that  such  a  condition,  comparable  to  the  de- 
magnetization of  a  magnet  by  a  blow  of  a  hammer, — a  favor- 
ite simile  of  Erichsen's — was  ever  caused  by  direct  blows 
on  the  back  or  by  a  general  shaking  up  of  the  whole  body. 
He  fully  admitted  the  possibility  of  intraspinal  haemorrhage 
without  external  evidences  of  violence,  but  he  claimed  that 
such  injuries  occurred  in  a  relatively  small  proportion  of 
railway  cases,  and  did  not  need  to  be  explained  by  any 
theory  of  molecular  disarrangement.  The  larger  number 
of  Page's  cases  had  received  slight  injuries,  and  the  symp- 
toms which  came  on  immediately  or  soon  after  the  accident 
consisted  chiefly  of  pain  in  the  back,  associated  with  the 
common  subjective  disorders  of  neurasthenia,  but   without 


HISTORY   OF    THE    TRAUMATIC    NEUROSES. 


193 


any  of  the  localizing  signs  of  organic  injury.  He  also  rec- 
ognized the  existence  of  disturbances  of  motion  dependent 
upon  idea  or  loss  of  will  power.  His  chapter  on  functional 
or  neuromiinetic  disorders  gives  several  interesting  cases 
which  would  to-day  be  called  traumatic  hysteria.  One  of 
these  may  be  quoted  to  show  the  long  duration  which  is 
possible  in  functional  paralysis  : 

"Case  of  functional  motor  paraplegia.  Extreme  emotional  dis- 
turbances." Man,  aged  forty-one,  who  was  naturally  very  excita- 
ble, was  in  a  very  severe  collision  in  which  the  carriage  he  was  in 
was  smashed  to  pieces.  There  were  no  evidences  of  severe  phys- 
ical injury,  but  the  patient  was  very  nervous  and  in  bed  for  sev- 
eral days.  Complained  of  pain  in  the  back.  No  tenderness.  He 
dwelt  on  the  fear  of  paralysis,  and  steadily  lost  power  in  the  legs. 
Eight  months  after  the  accident  he  was  quite  unable  to  walk,  and 
failed  entirely  to  make  any  requested  movements  of  the  legs  or 
feet  during  examination.  There  was  no  paralysis  of  bowels  or 
bladder,  and  the  sensory  impairment  was  at  best  slight.  There 
were  no  bed  sores  or  atrophy  of  muscles. 

Nine  months  after  the  accident  the  patient  had  a  sudden  at- 
tack of  aphonia,  which  lasted  three  weeks  and  disappeared  as 
suddenly  as  it  came.  He  was  troubled  by  excessive  emotional 
irritability.  Page's  report  to  the  company,  nine  months  after  the 
accident  was,  that  "the  cause  of  the  paralysis  seems  to  lie  in  the 
directing  power  of  the  will,  rather  than  in  lesion  discoverable  of 
the  brain  or  spinal  cord."  The  man  ultimately  recovered,  but 
was  ill  four  to  five  years.  His  recovery  came  suddenly.  He  had 
been  unable  to  get  out  of  his  chair  without  help  until  one  day  he 
got  up  without  knowing  it.  His  son  said  to  him,  "Why,  father, 
look  what  you've  done!"  "Good  God,"  he  replied,  I  have  got 
up  myself !  "     From  that  day  he  could  get  up  without  difficulty. 

Page  publishes  an  appendix  to  his  book,  in  which  are 
tabulated  the  ultimate  results  of  two  hundred  and  thirty-four 
cases  as  observed  from  two  to  five  years  after  the  accident. 
He  says  that  most  cases  recover  completely,  although  re- 
covery  may  be  much  delayed. 

He  admits,  however,  that  the  injured  man  may  never  be 
as  well  as  he  was  before,  and  that  many  patients   perma- 


IQ4  FU^XTIOXAL    EFFECTS    OF    IN'JURY. 

nently  retain  evidences  of  impaired  health.  From  an  exam- 
ination of  his  table  it  would  seem  that  complete  recovery 
did  not  occur  in  more  than  seventy  per  cent  of  the  cases. 

Page's  book  quickly  obtained  wide  favor,  and  a  second 
edition  appeared  in  1885.  At  this  time,  also,  the  possibility 
of  hysteria  occurring  as  a  result  of  injury  and  shock  became 
recognized,  and  attention  was  called  to  the  fact  that  some 
of  the  cases  of  "  concussion  of  the  spine  "  were  purely  hys- 
terical. Putnam  had  an  accident  case  of  hysterical  hemi- 
analgesia  and  paraplegia,  and  emphasized  the  necessity  of 
looking  for  hysteria  in  all  concussion  cases.  Walton  re- 
ported a  case  of  hysterical  anaesthesia  brought  on  by  a  fall, 
and  in  an  article  entitled  "  Spinal  Irritation  "  he  suggested 
a  probable  cerebral  origin  for  many  of  the  symptoms  of 
these  disorders,  and  proposed  the  term  "  railway  brain  "  as 
a  substitute  for  "railway  spine."  Dana,  in  December,  1884, 
gave  the  first  complete  re'siune  of  these  disorders.  His  con- 
clusions— which,  with  very  slight  modifications,  have  been 
proved  to  be  correct — are  :  "  That  the  term  spinal  concussion 
is  misleading  and  often  incorrect,  and  the  symptoms  which 
are  usually  associated  with  that  name  are  really  symptoms 
of  traumatic  neurasthenia,  hysteria,  and  hypochondriasis, 
associated  more  or  less  with  symptoms  of  injury  to  the  ver- 
tebral muscles  and  Hgaments  and  to  the  spinal  nerves ;  that, 
in  other  words,  concussion  is  mental  shock  and  physical 
bruising."  Dana  beheved  in  "  concussion  of  the  spine  "  as 
occurring  in  rare  instances,  and  recognized  the  possibility  of 
injuries  and  jars  causing  myelitis  without  there  being  any 
injury  to  the  spinal  column. 

In  the  following  year,  Thomsen  and  Oppenheim,  assist- 
ants of  Westphal,  in  support  of  the  theory  of  an  organic 
basis  for  these  disorders,  maintained  that  hemianeesthesia 
was  not  a  pathognomonic  symptom  of  hysteria,  but  might 
result  from  organic  cerebral  injury,  and  consequently  could 
not  be  regarded  as  proof  that  many  of  these  cases  were  not 


HISTORY   OF    THE    TRAUMATIC   NEUROSES.  195 

oro-anic  in  character.  It  must  be  remarked,  however,  that 
the  cutaneous  insensibility  studied  by  these  authors  in  pa- 
tients suffering  from  cerebral  disease  differed  in  essential 
particulars  from  the  hemianassthesia  of  hysteria.  It  oc- 
curred as  a  general  hypalgesia,  or  diminution  of  sensibility 
to  pain,  which  was  more  marked  on  one  side  than  on  the 
other,  rather  than  in  the  form  of  the  sharply  defined  uni- 
lateral loss  of  sensation  so  commonly  observed  in  hysteria. 
Also,  nearly  all  the  cases  examined  by  them  presented 
psychical  anomalies — hallucinations,  apathy,  depression,  etc. 
— conditions  which  render  any  examination  of  sensations, 
unsatisfactory  and  unreliable.  Consequently,  the  paper  by 
these  authors  can  in  no  way  be  regarded  as  overthrowing 
the  theory  of  a  hysterical  character  for  many  of  the  trau- 
matic affections  under  discussion.  In  1885  Oppenheim  re- 
turned to  the  views  of  Westphal — namely,  that  the  symp- 
toms of  "  railway  brain  "  were  due  to  disseminate  foci  of 
inflammation  or  softening. 

Striimpell,  writing  in  1888,  described  a  general  traumatic 
neurosis  and  a  local  traumatic  neurosis. 

The  general  traumatic  neurosis,  which  is  apparently  a 
mixture  of  hysteria  and  neurasthenia,  he  illustrates  as  fol- 
lows: 

A  healthy  man  falls  from  a  height,  is  unconscious  or  dazed, 
and  has  to  be  carried  home.  There  are  no  serious  injuries  dis- 
coverable. Recovery  is  very  slow,  and  the  patient  stays  in  bed 
for  some  time.  Then  he  finds  himself  unable  to  work.  He  be- 
comes very  nervous.  He  is  melancholy  and  depressed,  and  ceases 
to  take  an  interest  in  his  surroundings.  He  loses  his  energy  and 
will  power,  and  becomes  agitated  on  slight  provocation.  There 
may  be  considerable  loss  of  memory.  There  is  difficulty  in  fixing 
and  holding  the  attention.  Sleep  is  disturbed  by  dreams.  There 
are  cutaneous  anaesthesia  and  hyperaesthesia  (especially  of  the 
back),  and  there  may  be  a  dissociation  of  sensations.  The  func- 
tion of  the  special  senses  is  impaired. 

The  motor  difficulties  consist  in  weakness  rather  than  pa- 
ralysis. 


iq5  functional  effects  of  injury. 

Tremor  and  stiffness  of  the  muscles  are  frequently  present. 
The  skin  reflexes  are  often  absent,  and  the  deep  reflexes  are  gen- 
erally exaggerated.  There  are  various  functional  disturbances  of 
the  vegetative  organs,  and  complaints  are  made  of  loss  of  sexual 
inclination  and  power.     Many  of  these  cases  are  incurable. 

Under  the  head  of  local  traumatic  neurosis  Striimpell  de- 
scribed the  various  local  manifestations,  such  as  paralysis, 
contracture,  hyperaesthesia,  joint  affections,  etc.,  of  hysteria. 

Interest  in  the  causative  relation  of  trauma  to  nervous 
disease  reached  its  height  when,  in  1889,  Oppenheim  pub- 
lished his  celebrated  monograph,  Die  traumatiscJie  Neurosen 
(The  Traumatic  Neuroses),  a  book  v^^hich  has  been  widely 
read  and  which  has  exerted  no  little  influence  upon  subse- 
quent discussions  of  nervous  disorders  following  accidents. 
Oppenheim  did  not  attempt  any  description  of  direct  lesions 
of  the  nervous  system.  He  only  delineated  the  clinical  forms 
which  result  from  accident  and  injury  and  which  affect  the 
nervous  system  "  through  sudden  vibration  or  in  reflex 
ways."  He  admitted  the  existence  of  traumatic  hysteria  and 
traumatic  neurasthenia,  but  to  the  forms  of  functional  trau- 
matic disorder,  which  are  not  typical  for  either  hysteria  or 
neurasthenia,  he  gave  the  name  of  traumatic  neurosis. 

The  symptoms  of  Oppenheim's  traumatic  neurosis  are 
chiefly  a  combination  of  the  symptoms  of  severe  neurasthe- 
nia, with  some  hysterical  manifestations.  They  may  develop 
immediately  after  an  accident,  or  their  appearance  may  be 
delayed  for  weeks  or  months.  The  first  disturbances  are 
purely  subjective,  such  as  pains  in  the  back  or  headache, 
anxiety,  and  restlessness.  Depression  and  general  worry 
may  amount  to  hypochondriasis,  without,  however,  direct 
impairment  of  the  mental  power.  The  patients  are  sleepless, 
dizzy,  and  subject  to  "  weak  spells  "  ;  they  have  bad  dreams  ; 
tremor  occurring  as  a  simple  vibration,  or  in  the  form  of  tic 
convulsif,  chorea,  epilepsy,  etc.,  are  not  infrequently  observed. 
Disturbances  of  voluntary  motion  may  usually  be  explained 


HISTORY   OF   THE   TRAUMATIC   NEUROSES. 


197 


by  pain  caused  by  movement,  though  the  muscles  are  nearly 
always  weak  and  may  be  entirely  paralyzed ;  there  may 
be  a  weakness  of  all  four  extremities,  or  hemiparesis,  or 
paraparesis,  or  monoparesis ;  the  paralysis  differs  from 
organic  paralysis  in  important  particulars,  one  of  which 
is  a  peculiar  rigidity  of  the  muscles.  The  knee-jerks  are 
frequently  exaggerated,  but  never  lost.  Atrophy  may 
occur. 

Disorders  of  speech  are  limited  to  a  form  of  stuttering. 
Inequality  of  the  pupils  is  frequent,  but  they  rarely  fail  to 
react  to  light.  Loss  of  sensibility  of  the  skin  and  mucous 
membranes  occurs,  but  does  not  follow  the  distribution  of 
organic  angesthesia.  The  visual  fields  may  be  contracted. 
Vaso-motor  disturbances  are  prominent.  The  bladder  is 
rarely  involved,  although  there  may  be  difficulty  in  passing 
water,  or  incontinence  or  retention  of  urine.  The  sexual 
function  is  generally  impaired.  The  condition  of  the  skin 
reflexes  is  not  constant.  They  may  be  active,  but  are  usu- 
ally diminished  or  lost  in  anaesthetic  areas.  Cardiac  irrita- 
bility is  frequent.  Oppenheim  deduces  the  symptomatology 
from  forty-two  cases  which  he  had  observed.  Very  few  of 
the  patients  entirely  recovered. 

Oppenheim's  monograph  was  followed  by  the  appear- 
ance in  America  of  a  book  by  Clevenger,  of  Chicago,  enti- 
tled Spinal  Concussion.  Clevenger  proposed  the  name  of 
"  Erichsen's  disease  "  for  these  disorders.  He  says:  "  Erich- 
sen's  disease  is  a  group  of  mainly  subjective  symptoms  of  a 
nervous  and  mental  nature,  sufficiently  characteristic  to  en- 
able it  to  be  recognized  as  a  traumatic  neurosis,  distinct 
from  other  traumatic  neuroses,  with  which  it  may  or  may 
not  be  associated.  The  most  common  cause  of  Erichsen's 
disease  is  a  concussion  of  the  spinal  column,  including  its 
contents  and  nearest  appendages." 

The  term  "  Erichsen's  disease  "  has  not  met  with  favor 
-as  a  designation  for  any  symptom  group,  and  Clevenger's 
14 


iq8  functional  effects*of  injury. 

work  is  said  by  Gilles  de  la  Tourette  to  be  "  le  triompJie  de  la 
confusio7i  des  idees  en  pareille  matured 

Since  1889  the  neuroses  following  accident  or  injury  have 
been  a  subject  of  contention,  especially  among  neurologists. 
The  views  of  Striimpell  and  Oppenheim  created  much  dis- 
cussion. By  some  the  existence  of  a  special  traumatic  neu- 
rosis with  characteristic  symptoms  was  unreservedly  ac- 
cepted. Many  indorsed  the  theory  with  certain  modifica- 
tions, and  a  few  spoke  emphatically  against  the  individuality 
of  any  neurosis  which  occurs  only  as  a  result  of  injury  and 
shock. 

Eisenlohr  and  Schultze,  especially,  questioned  the  value  of 
the  individual  symptoms  upon  which  rested  the  theory  of  a 
clinical  entity  for  a  special  neurosis  after  trauma.  Schultze 
declared  that  "  while  a  variety  of  neuroses  and  psychoses 
may  be  induced  by  trauma,  the  traumatic  neurosis  as  such 
has  no  existence."  Bruns  also  adopted  this  view,  believing 
it  more  correct  to  make  the  diagnosis  of  traumatic  hysteria 
or  traumatic  neurasthenia  than  to  speak  of  a  traumatic  neu- 
rosis. But  Bruns  admitted  that,  even  after  the  most  careful 
efforts  at  differential  diagnosis  between  the  various  neuroses 
of  traumatic  origin,  there  remained  a  certain  number  of 
mixed  forms  which  can  not  be  satisfactorily  classified. 

The  opposition  to  the  admission  into  medicine  of  a  trau- 
matic neurosis  as  a  distinct  disorder  became  more  and  more 
pronounced.  At  the  Twelfth  International  Medical  Con- 
gress, held  at  Wiesbaden  in  1893,  it  was  generally  accepted 
"  that,  even  after  slight  injuries,  general  functional  disorders 
not  infrequently  develop.  These  neuroses  are  not  disease 
pictures  of  any  particular  variety,  but  all  may  be  classified 
under  the  name  of  other  well-recognized  neuroses,  of  which 
the  most  important  are  hysteria,  neurasthenia,  hypochon- 
driasis, and  their  mixtures." 

The  literature  of  the  traumatic  neuroses  is  now  very  large. 
Page,  in  1891,  published  a  new  and  shorter  book.     In  this 


HISTORY    OF    THE    TRAUMATIC    NEUROSES.  igg 

country  Knapp  has  embodied  the  results  of  his  extensive 
study  and  experience  in  an  excellent  chapter  in  the  Text- 
book of  Nervous  Diseases  by  American  Authors.  Dana  also 
discusses  the  subject  very  thoroughly  in  Hamilton's  Text- 
book of  Legal  Medicine.  Dr.  Outten,  in  Witthaus's  Medical 
Jurisprudence,  writes  with  an  authority  acquired  through 
large  experience  as  a  railway  surgeon.  Crocq  has  written 
an  essay  on  the  "  Nevroses  traumatiques,"  which  has  been 
crowned  by  the  Belgian  Academy.  An  able  summary  of 
the  questions  involved  has  been  given  by  Saenger. 

Striimpell  recently  has  cast  doubt  upon  the  value  of 
many  of  the  individual  symptoms  of  the  traumatic  disorder. 
His  new  position  was  attacked  by  the  men  who  took  part  in 
the  discussions  at  Hamburg  and  Frankfort  in  the  spring  and 
summer  of  1896. 

Such  is  the  history  of  the  views  regarding  the  functional 
nervous  disorders  which  most  commonly  follow  railway  and 
allied  injuries.  From  the  time  that  they  were  recognized  as 
depending  upon  functional  nervous  disturbance,  of  which 
the  structural  changes  are  more  minute  and  more  baffling 
than  the  coarse  lesions  of  haemorrhage,  softening,  or  inflam- 
mation, they  became  the  object  of  study  by  neurologists 
rather  than  by  surgeons. 

Discussions  concerning  them  have  been  held  with  activ- 
ity and  at  times  with  acerbity.  It  is  not  surprising  that, 
without  the  guidance  of  visible  pathological  anatomy,  the 
views  of  different  observers  regarding  the  nature  of  symp- 
toms are  not  entirely  unanimous.  But  the  progress  of  gen- 
eral neurology  has  been  constant,  and  year  by  year  our  un- 
derstanding of  the  genesis  and  character  of  these  neuroses 
becomes  clearer.  To-day,  although  not  perfectly  understood 
nor  classified  with  absolute  security,  they  have  obtained  a 
firmer  foothold  in  clinical  medicine  than  they  ever  had 
before. 

The  larger  number  of  cases  can  be  made  to  agree  with 


200  FUNCTIONAL   EFFECTS   OF   INJURY. 

well-recognized  and  well-defined  clinical  types,  so  that  the 
course  of  any  individual  case  can  be  foretold  with  a  certain 
degree  of  accuracy. 

The  following  is  a  summary  of  the  present  understand- 
ing of  the  essential  features  of  the  traumatic  neuroses  : 

Nomenclature. — There  is  now  a  nearly  complete  una- 
nimity of  opinion  that  there  is  no  such  thing  as  a  special 
neurosis  excited  by  trauma.  Injury  and  shock  may  be  fol- 
lowed by  symptoms  of  any  of  the  well-recognized  neuroses 
or  psychoses,  or  the  symptoms  of  one  or  more  of  these  dis- 
orders may  be  blended  in  the  same  case.  But  the  theory  of 
a  special  traumatic  neurosis  lacks  clinical  foundation  and 
has  been  generally  abandoned.  Even  the  severe  forms  of 
nervous  disturbance  which  sometimes  follow  injury,  the  ob- 
servation of  which  led  Oppenheim  to  coin  the  term  "  trau- 
matic neurosis,"  do  not  need  to  be  explained  by  assigning 
them  to  a  special  nosological  place  of  their  own.  Some  of 
them  are  mixtures  of  hysteria  and  neurasthenia,  and  others 
may  eventually  be  shown  to  depend  upon  structural  changes 
in  the  central  nervous  system,  of  which  the  clinical  manifes- 
tations are  associated  with  symptoms  of  hysteria  and  neu- 
rasthenia. These  cases  present  no  symptoms  which  can  not 
be  explained  on  such  an  hypothesis.  There  is  nothing  suffi- 
ciently individual  about  them  to  warrant  the  use  of  the  term 
"  the  traumatic  neurosis." 

If  this  view  is  correct,  if  there  is  no  individual  traumatic 
neurosis,  and  if  trauma  is  to  be  regarded  in  this  connection 
merely  as  an  exciting  cause  of  other  well-known  nervous  dis- 
orders of  functional  character,  the  comprehensiveness  of  the 
term  traumatic  neuroses  might  be  very  much  enlarged. 
Besides  neurasthenia  and  hysteria  with  their  mixtures  and 
allies,  and  possibly  some  forms  of  organic  disease  whose 
pathology  is  still  to  be  explained,  it  could  include  neuralgia, 
chorea,  exophthalmic  goitre,  or  any  disease  which  is  a  neu- 
rosis and  which  may  develop  as  a  result  of  injury  and  shock. 


NOMENCLATURE   OF   THE   TRAUMATIC   NEUROSES.      201 

Such  a  nomenclature  would,  however,  be  entirely  at  vari- 
ance with  the  original  significance  of  the  term  and  would 
leave  us  without  any  generic  designation  under  which  to 
classify  the  forms  of  functional  nervous  disease  which  have 
obtained  such  prominence  in  medical  jurisprudence.  For 
the  present,  at  least,  it  seems  impossible  to  dispense  with  an 
expression  which,  although  inexact,  has  come  to  be  gener- 
ally recognized  as  applying  only  to  a  particular  class  of 
cases.  But,  while  retaining  "  traumatic  neuroses  "  as  a  gen- 
eric designation,  the  physician  should  not  be  satisfied  in 
saying  of  any  given  case  that  it  is  one  of  the  traumatic  neu- 
roses, but  should  continue  the  examination  until  he  can  say, 
in  all  probability  at  least,  which  one.  It  is  only  by  repeated 
efforts  at  exclusive  diagnosis  that  the  pathology  and  classi- 
fication of  these  disorders  will  be  rendered  still  more  plain. 

Striimpell  has  suggested  that  "  traumatic  neuroses  "  be 
changed  to  "  accident  neuroses."  Against  this  may  be 
urged  that  they  do  not  necessarily  result  from  accidents. 
Injuries  received  in  battle  can  hardly  be  called  accidental. 
Strlimpell's  reason  for  the  substitution  of  "  accident  "  was 
because  a  trauma  is  not  always  demonstrable.  But  the 
wider  definition  of  trauma  includes  psychic  as  well  as  ph3'S- 
ical  injury,  and  consequently  traumatic  can  be  with  propri- 
ety applied  to  those  neuroses  which  result  from  psychic 
shock  as  well  as  from  physical  injury. 

In  the  following  pages  these  disturbances  will  be  dis- 
cussed under  the  heads  of — 

1.  Traumatic  neurasthenia. 

2.  Traumatic  hysteria. 

3.  Unclassified  forms. 

In  traumatic  neurasthenia  the  mental  state  is  subject  to 
wide  variations.  The  disorder  may  take  on  the  type  of  hy- 
pochondriasis, less  frequently  that  o^  melancholia.  These 
variations  will  be  here  described  as  variations  of  a  common 
morbid  condition. 


202  FUNCTIONAL   EFFECTS   OF   INJURY. 

Hysteria  following  traumata  is  not  always  of  the  pure 
type  seen  when  the  affection  develops  in  young  women  from 
non-traumatic  causes.  When  owing  its  origin  to  injury  or 
fright,  it  is  more  commonly  associated  with  pronounced 
neurasthenic  symptoms,  such  as  are  usually  present  in  non- 
traumatic hysteria  occurring  in  men.  Although  traumatic 
neurasthenia  and  traumatic  hysteria  frequently  occur  to- 
gether (traumatic  hystero-neurasthenia),  for  purposes  of  con- 
venience they  will  be  described  separately. 

The  uncertainty  regarding  the  group  of  cases  called  un- 
classified is  explained  by  the  name.  Further  information  is 
necessary  before  they  can  be  assigned  to  any  nosological 
category.  To  the  other  functional  nervous  disorders,  which 
are  neuroses,  and  which  may  arise  from  trauma,  such  as 
exophthalmic  goitre,  chorea,  etc,  no  mention  will  be  made. 
They  are  not  included  by  the  general  term  "  traumatic  neu- 
roses," and  require  no  description  in  a  work  of  this  char- 
acter. 

Pathology. — The  possibility  of  injury  to  nervous  tissue 
has  already  been  considered  in  Part  I. 

The  belief,  which  was  first  systematically  formulated  by 
Page,  has  now  become  general,  that  in  by  far  the  larger  num- 
ber of  litigated  cases  of  nervous  disorders  which  follow  rail- 
way and  allied  accidents  there  is  no  gross  injury  to  nervous 
tissue.  Physical  concussion  may  be  a  cause  of  subjective 
nervous  symptoms,  and  if  severe  may  indirectly  cause  or- 
ganic injury.  But  the  conception  of  spinal  concussion  as 
a  cause  for  general  nervous  symptoms  and  as  a  pathological 
condition  is  without  foundation  and  has  been  almost  en- 
tirely abandoned.  By  far  the  larger  number  of  cases  of  the 
traumatic  neuroses  may  be  explained  by  the  theory  that  the 
symptoms  are  those  of  hysteria  or  neurasthenia,  functional 
disorders  of  which  the  pathology  is  unknown.  There  are, 
however,  a  few  cases  in  which  the  symptoms  are  somewhat 
different  from  those  of  hysteria  and  neurasthenia,  and  which 


ETIOLOGY   OF   THE   TRAUMATIC   NEUROSES. 


203 


may  depend  upon  the  structural  lesions  of  the  brain  and 
spinal  cord,  although  our  knowledge  concerning  their  pa- 
thology is  still  largely  speculative. 

iEtiology. — There  are  so  many  causative  factors  common 
to  all  of  the  neuroses  of  traumatic  origin  that  they  may  best 
be  described  in  a  general  way  together.* 

Accidents  which  become  the  subject  of  medico-legal  in- 
quiry are  more  frequently  followed  by  functional  nervous 
disorders  than  by  organic  injuries  to  the  nervous  system. 
An  analysis  of  one  hundred  successive  cases  which  were 
seen  by  Walton,  where  nervous  symptoms  were  complained 
of  and  in  which  the  question  of  damages  had  arisen  or  were 
likely  to  arise,  gives  the  following  results.  "  The  date  of  the 
examination  was  from  one  week  to  three  and  a  half  years 
after  the  accident,  and  the  nature  of  the  trauma  ranged  from 
slight  jars  and  moderate  blows  on  various  parts  of  the  body, 
to  violent  collisions  and  severe  falls.  In  seventeen  cases 
there  were  unmistakable  evidences  of  injury  to  the  spinal 
cord.  In  the  remaining  cases  the  symptoms,  although  often 
in  many  cases  pronounced,  differed  in  essential  respects  from 
the  symptoms  of  organic  nervous  diseases." 

Although  the  traumatic  neuroses  may  follow  any  acci- 
dent in  which  injury  and  shock  have  been  prominent  fac- 
tors, they  have  been  chiefly  studied  in  connection  with  rail- 
way accidents. 

Interest  in  them  has  advanced  with  the  extension  of  rail- 
way travel,  and  until  1866  little  attention  had  been  given  to 
these  disorders.  It  is  only  in  recent  years  that  railway 
travel  has  assumed  proportions  sufficiently  extensive  to  cre- 
ate for  railway  injuries  a  medical  literature  of  their  own.  Im- 
proved mechanical  appliances,  perfected  systems  of  signals, 
and  the  enforcement  of  military  discipline  among  employees 

*  Causal  characteristics  special  to  any  individual  form  will  be  given  under  its 
description. 


204  FUNCTIONAL   EFFECTS   OF   INJURY. 

all  tend  to  reduce  the  accident  percentage.  But  these  ad- 
vances are  more  than  counterbalanced  by  the  constantly 
increasing-  traffic  on  all  kinds  of  surface  vehicles,  so  that  the 
number  of  persons  killed  and  injured  becomes  constantly 
larger. 

The  following  table  is  taken  from  the  Eighth  Annual  Re- 
port of  the  Interstate  Commerce  Commission  (Washington,. 
1896).  It  contains  the  total  number  of  persons  killed  and 
wounded  on  railways  in  the  United  States  during  the  last 
eight  years : 

Comparative  Summary  of  Railway  Accidents  for  the  Years  ending 
Jime  JO,  i8g_5,  i8g4,  iSgj,  i8g2,  i8gi,  i8go,  i88g,  and  1888. 


EMPLOYEES. 

PASSENGERS. 

OTHER  PERSONS. 

TOTAL. 

Year. 

Killed. 

Injured. 

Killed. 

Injured. 

Killed. 

Injured. 

Killed. 

Injured- 

iSot;              

1,811 

2i;.6o6 

170 
324 

2,375 

';,0'^4 

4,155 
4,300 

4>320 

4,217 
4,076 
3-598 
3,541 
2,897 

5.677 
5,433 
5,435 
5,158 

4,769 
4,206 

4.135 
3,602 

6,136 
6,447 
7.346 
7,147 
7,029 

6,335 
5,823 
5,282 

33,748 

TRnjL       

1,823:  23,422 

2,727   31.729 
2,554   28,267 
2,660   26,140 
2,451    22,396 
1,972    20,028 
2,070  20.148 

31,889 

iSna       

299:     3,229 
376      3,227 
293      2,972 
286      2,425 
310      2,146 
315!     2,138 

40,393 

1892       

36,652 

1891        

33.881 

iggo         

29,027 

I8S9         

26,309 

1888                 

25,888 

1 

1 

After  allowance  has  been  made  for  the  increased  number 
of  accidents  in  1893,  the  year  of  the  World's  Fair,  during 
which  travel  was  very  extensive,  it  will  be  seen  that  the  total 
number  of  persons  killed  and  injured  during  the  past  four 
years  is  considerably  larger  than  during  the  four  preceding 
years.  Startling  as  are  these  figures,  many  deaths  and  casu- 
alties may  properly  be  classed  as  occurring  on  railways, 
which  do  not  appear  in  this  report. 

The  extension  of  the  means  of  rapid  surface  transporta- 
tion in  recent  years  has  very  much  widened  the  conception 
of  the  term  railway.  It  now  includes  elevated  roads,  elec- 
tric systems  of  all  kinds,  cable  roads,  and  to  a  certain  extent 
horse-car  lines. 

Railway  collisions  or  derailments   are  particularly  well 


^ETIOLOGY    OF   THE^  TRAUMATIC   NEUROSES.  205 

adapted  to  cause  every  variety  of  injury.  Decapitation, 
dismemberment,  bruises  and  crushes  of  the  fiesh,  fractures, 
dislocations  and  twists  of  the  bones  and  joints,  cuts  from 
broken  glass,  burns  and  scalds  from  fire  and  escaping  steam, 
may  immediately  induce  death  or  cause  disabilities  and  dis- 
figurements of  all  degrees.  To  the  physical  dangers  of  such 
disasters  is  added  mental  shock.  It  is  needless  to  emphasize 
how  lasting  must  be  the  terrible  impression  which  is  made 
by  the  suddenness  of  the  accident,  the  ebranlement,  the  crash 
of  breaking  wood  and  glass,  the  cries  of  the  wounded,  the 
noise  of  escaping  steam,  and  the  uncertainty  and  terror  of 
such  catastrophes.  But  while  death  or  physical  injuries  of 
every  character  and  degree  may  result  from  these  acci- 
dents, the  number  of  persons  who  receive  in  this  way  or- 
ganic injury  of  the  nervous  system  is  not  great  when  com- 
pared with  the  number  of  persons  who,  although  hurt  but 
little  or  not  at  all  at  the  time  of  the  accident,  eventually 
develop  some  nervous  symptoms.  It  is  a  matter  of  general 
remark  that  the  functional  disorders  occur  most  frequently 
when  there  has  been  no  gross  physical  injury.  In  railway 
accidents  there  are  usually  a  large  number  of  persons  who 
neither  die  nor  yet  are  badly  hurt.  They  may  be  severely 
frightened,  and  violently  thrown  about,  and  receive  twists 
or  wrenches  of  the  spine,  or  blows  upon  the  back  or  head. 
But  whatever  physical  injury  is  incurred,  it  does  not  cause 
them  great  pain  or  disability  at  the  time.  Yet  it  is  these 
persons  who  were  considered,  at  the  time  of  the  accident, 
as  fortunate  in  escaping  unscathed  or  with  slight  injury, 
who  eventually  complain  of  the  symptoms  of  some  one  of 
the  traumatic  neuroses.  There  is  no  reason  to  suppose  that 
in  such  cases  the  nervous  system  has  received  any  structural 
damage,  for  in  organic  nervous  injury  there  is  almost  im- 
mediate loss  of  nervous  function.  In  the  traumatic  neu- 
roses, on  the  other  hand,  with  the  exception  of  some 
cases  of  hysteria,  there  is  an  interval  between  the  occur- 


2o6  FUNCTIONAL   EFFECTS   OF    INJURY. 

rence  of  the  accident  and  the  appearance  of  pronounced 
symptoms. 

In  many  cases  actions  for  personal  injuries  are  brought 
when  there  has  not  only  been  no  physical  injury,  but  even 
when  there  has  been  no  general  accident.  The  sudden 
starting  or  stopping  of  a  train,  the  slipping  in  an  aisle  or 
from  steps  covered  with  ice,  or  similar  trivial  mishaps,  are 
alleged  as  causes  of  neurasthenic  symptoms.  A  woman  in 
Brooklyn  recently  brought  suit  for  ten  thousand  dollars  for 
alleged  injuries  (none  were  visible)  received  by  being  thrown 
from  her  seat  to  the  floor  by  the  sudden  stopping  of  a  trol- 
ley car. 

But  although  many  escape  from  railway  accidents  with- 
out severe  physical  injury,  few  are  so  fortunate  as  not  to  be 
very  much  terrified  and  dazed.  Fright  is  as  fruitful  a  cause 
of  some  functional  nervous  disorders  as  physical  injury.  It 
alone  may  be  sufficient  to  induce  paralysis  agitans,  chorea,  or 
exophthalmic  goitre,  and  its  influence  as  a  causative  factor 
in  the  neuroses  which  most  frequently  become  the  subjects 
of  litigation — neurasthenia  and  hysteria — is  very  impor- 
tant. Any  of  the  manifestations  of  hysteria  may  appear 
for  the  first  time  as  a  result  of  fright  or  nervous  shock 
alone.  As  we  shall  see  in  speaking  of  the  setiology  of  trau- 
matic neurasthenia,  fright  is  usually  associated  with  some 
physical  injury  in  the  causation  of  that  disorder,  although 
the  physical  commotion  or  shock  may  be  very  slight.  Both 
traumatic  neurasthenia  and  traumatic  hysteria  may  some- 
times seem  to  be  the  result  of  physical  injury  alone  or  of  psy- 
chic shock  alone,  but  in  by  far  the  larger  number  of  cases  of 
these  diseases  the  two  causative  factors  have  been  active  ; 
and  the  fact  that  in  catastrophes  which  occur  on  railways 
large  numbers  of  persons  are  subjected  to  fright  and  to  some 
physical  commotion,  explains  in  part  why  railway  accidents 
are  such  fertile  causes  of  these  disorders. 

Although  accidents  on  railways  stand  in  the  most  con- 


ETIOLOGY   OF   THE    TRAUMATIC   NEUROSES.  207 

spicuous  causal  relation  to  some  of  the  traumatic  neuroses, 
any  of  these  disorders  may  follow  mishaps  or  catastrophes 
of  diverse  character  in  which  the  elements  of  physical  com- 
motion or  injury,  and  psychic  shock,  are  prominent. 

New  inventions  and  elaborated  mechanical  contrivances 
are  constantly  supplying  additional  causative  factors.  They 
may  follow  accidents  in  elevators,  in  theatres,  in  machine 
shops.  The  introduction  of  rapid  surface  transit  in  the  streets 
has  caused  the  annual  number  of  these  disorders  to  very  ma- 
terially increase. 

The  rapid  development  in  recent  years  of  the  industrial 
uses  of  electricity  has  added  another  to  the  already  long  list 
of  exciting  causes.  Electric  currents  of  high  potential  are 
now  of  such  indispensable  service  in  city  life  that  the  danger 
of  receiving  shocks  from  street  currents,  although  chiefly 
limited  to  electric  linemen,  is  one  to  which  every  citizen  is 
more  or  less  exposed.  It  is  not  probable  that  electric  cur- 
rents which  do  not  induce  almost  instant  death  ever  cause 
organic  nervous  disease.  No  such  case  has  ever  come  to 
my  personal  observation,  and  a  search  through  literature  for 
the  record  of  such  a  case  has  proved  fruitless.  As  far  as  the 
nervous  system  is  concerned,  it  is  the  functional  affections 
which  result  from  accidents  by  electricity,  and  it  is  the  gen- 
eral public,  rather  than  the  employee  of  the  company,  which 
suffers.*  The  lineman  may  be  seriously  burned  or  be  in- 
stantly killed  by  touching  live  wires  or  by  receiving  in  vari- 
ous ways  currents  of  high  voltage.  But  he  resembles  the 
brakeman  in  this  respect,  that  he  receives  his  injury  and  dies 
of  it,  or  quickly  gets  over  the  effects  of  it.  Constant  famil- 
iarity has  so  eliminated  the  element  of  fright  that  for  him  it 
is  a  physical  injury,  and  rarely  is  followed  by  any  symptoms 
of  functional  nervous  disease.      In  persons  unfamiliar  with 

*  In  New  York  city,  the  placing  of  the  electric-light  wires  underground,  which 
was  brought  about  largely  by  the  efforts  of  H.  P.  Brown,  Esq.,  has  very  materially 
diminished  the  number  of  electrical  accidents  to  the  general  public. 


2o8  FUNCTIONAL   EFFECTS   OF   INJURY. 

electrical  appliances  the  effects  of  powerful  electrical  shocks 
are  essentially  different  from  those  experienced  by  the  em- 
ployees of  electrical  companies.  Such  a  one  who  touches 
or  is  touched  by  a  conductor  which  is  not  insulated,  or 
which  he  supposes  to  be  not  insulated,  receives,  independ- 
ently of  any  electric  shock,  a  fright  as  severe  as  the  fright 
caused  by  a  railway  collision.  Thus  a  case  is  reported 
by  Dana  of  a  patient  who  had  read  of  the  killing  of  a  man 
by  an  electric  wire.  A  few  days  after,  he  was  walking 
along  the  street  when  suddenly  a  dead  wire  fell  and  hit 
him  on  the  head.  The  blow  was  not  very  severe,  but  the 
man  fell  unconscious,  and  when  he  was  aroused  he  was 
found  to  have  typical  hysterical  symptoms.  Of  all  the  cases 
of  neurasthenia  or  hysteria  which  have  followed  contact 
with  wires  carrying  high  voltage  currents,  in  only  a  few 
is  there  reason  to  suppose  that  the  full  strength  of  the  cur- 
rent passed  through  the  body.  It  is  very  difficult  to  de- 
termine the  exact  strength  of  current  necessary  to  cause  ex- 
tensive burns  or  instant  death.  In  the  executions  at  Sing 
Sing  the  currents  are  not  of  higher  voltage  than  some  of  those 
which  pass  through  city  streets,  yet  the  effects  of  them  on 
condemned  murderers  are  not  always  identical.  In  some 
of  the  men  death  has  been  almost  instantaneous,  without  any 
charring  or  burning  of  the  body.  In  others  the  flesh  has 
been  considerably  burned  before  life  was  pronounced  to  be 
extinct.  It  is  impossible  to  say,  simply  from  the  examination 
of  a  person  who  has  received  a  strong  electric  current,  how 
strong  the  current  was  which  passed  through  him.  It  may 
have  been  weak,  and  still  have  caused  extensive  burns,  or 
it  may  have  been  fatal,  without  leaving  external  physical 
traces.  It  is  certain  that  the  victim  of  an  accident  rarely  re- 
ceives the  full  strength  of  a  current  of  high  potential.  The  con- 
tact is  usually  imperfect  and  only  momentary,  and  the  larger 
part  of  the  effects  of  the  electricity  are  dissipated  without 
coming  in  contact  with  the  body  at  all.    Clinical  observation 


ETIOLOGY   OF   THE   TRAUMATIC   NEUROSES.  209 

shows  that  the  greater  number  of  persons  who  develop 
neurasthenia  or  hysteria  as  the  result  of  accidents  with  elec- 
tric wires  have  not  been  seriously  injured.  There  are  some- 
times burns  of  the  clothing  or  of  the  hands,  but  these  are 
rarely  severe,  and  more  often  are  entirely  absent ;  and  in 
many  cases  circumstantial  evidence,  or  the  evidence  of  wit- 
nesses, proves  that  the  patient  received  no  electric  current 
at  all. 

That  fright  is  a  most  important  element  for  the  occur- 
rence of  the  traumatic  neuroses  appearing  as  sequelse  of 
electrical  accidents  receives  additional  proof  from  the  almost 
universal  agreement  of  opinion  that  such  accidents  are  most 
frequently  followed  by  the  symptoms  of  hysteria,  the  fright 
neurosis  par  excellence.  Neurasthenia,  however,  is  sometimes 
the  result  of  real  or  supposed  injury  from  electrical  currents. 
Knapp  reports  such  a  case : 

A  coachman,  forty-two  years  of  age,  strong,  healthy,  coura- 
geous, and  not  at  all  nervous,  was  driving  a  team  of  horses 
which  fouled  a  live  wire  and  were  thrown.  He  got  out  and  freed 
the  horses,  but  probably  received  no  physical  shock.  He  was 
very  much  frightened,  though  he  was  not  thrown  down  himself, 
and  walked  home.  After  the  accident  he  slept  badly;  was  nerv- 
ous and  apprehensive.  There  was  a  marked  tremor  of  head 
and  hands,  loss  of  sexual  desire,  pain  in  back,  exaggeration 
of  knee-jerks,  and  rapid  heart  action.  After  a  duration  of  three 
months  these  symptoms  entirely  disappeared,  and  the  man  be- 
came as  well  as  ever.  They  were  symptoms  of  essentially  neu- 
rasthenic character,  and,  as  such,  are  not  of  the  most  common 
type  observed  after  electrical  accidents. 

In  gaining  new  causes,  the  traumatic  neuroses  have  not 
lost  old  ones.  Any  one  of  them  may  result  from  a  fall  from 
a  horse,  from  a  carriage,  or  from  slippery  steps,  or  falls  of 
any  kind  in  which  the  person  is  frightened  and  he  is  hurt 
or  his  back  is  twisted.  They  very  frequently  follow  falls  in 
which  the  victim  strikes  on  the  head,  on  the  back,  or  on 
the  buttocks.     Blows  of  any  kind,  but  especially  such  as 


2IO  FUNCTIONAL   EFFECTS   OF   INJURY. 

fall  Upon  the  head  or  the  back,  are  often  followed  by  func- 
tional nervous  symptoms. 

Meteorological  disturbances,  and  especially  lightning, 
are  frequently  the  cause  of  nervous  manifestations  in  per- 
sons of  a  neurotic  temperament,  and  sometimes  seem  to  be 
the  only  setiological  factor  for  well-marked  neuroses.  What 
has  been  said  in  regard  to  the  place  occupied  by  powerful 
electric  currents  among  the  exciting  causes  of  the  traumatic 
neuroses  may,  with  certain  modifications,  be  repeated  for 
lightning.  Like  high  potential  currents,  it  may  instantly 
kill,  or  cause  extensive  burns.  But  the  persons  who,  after 
lightning  strokes,  develop  any  of  the  traumatic  neuroses,  of 
which  in  this  connection  hysteria  is  the  most  frequent,  usu- 
ally bear  no  traces  of  physical  injury  and  probably  have  not 
been  struck  at  all. 

Seismic  phenomena  are  associated  with  the  two  factors — 
physical  vibration  or  violence,  and  fright — most  essential  for 
the  occurrence  of  the  traumatic  neuroses,  and  they  are  fre- 
quently followed  by  symptoms  of  functional  nervous  disease. 

Charcot  observed  typical  cases  of  hysteria  after  the 
earthquake  in  Nice.  The  earthquake  in  Charleston,  S.  C, 
and  vicinity,  in  1886,  was  followed  by  many  cases  of  func- 
tional nervous  disorder. 

Porcher  quotes  as  follows  the  report  which  a  physician 
of  Camden,  S.  C,  made  to  the  State  Board  of  Health  one 
month  after  the  earthquake  shocks  of  August  31,  1886: 

"  They  "  (the  earthquake  shocks)  "  at  first  naturally  cre- 
ated much  consternation  among  our  population,  and  have 
undoubtedly  had  a  very  deleterious  effect  upon  sick  and 
feeble  persons,  being  followed  by  much  nervous  prostration 
and  other  unpleasant  symptoms.  Even  upon  well,  robust 
people  their  effects  have  been  striking  in  some  instances. 
Some  have  described  their  sensations  as  similar  to  those  ex- 
perienced after  a  shock  from  an  electric  battery  ;  others  have 
experienced  a  very  marked  feeling  of  debility  in  their  lower 


ETIOLOGY   OF    THE   TRAUMATIC   NEUROSES.  211 

extremities ;  others  have  had  vertigo,  nausea,  etc.  Some, 
again,  who  were  not  affected  by  these  unpleasant  symptoms 
in  the  beginning,  are  now  troubled  by  them." 

From  the  various  medical  reports  of  these  earthquake 
shocks,  it  appears  that  most  of  the  nervous  symptoms  which 
developed  as  a  result  of  them  were  neurasthenic  in  char- 
acter. 

Hughes  observed,  after  the  St.  Louis  cyclone  of  1896, 
"  cases  of  parsesthesia,  hypersesthesia,  analgesia  and  hyste- 
roidal  shock,  neurasthenia  and  some  of  the  so-called 
traumatic  neuroses,  and  '  railway-spine '  symptoms,  such 
as  follow  the  perceptibly  uninjured  after  railway  acci- 
dents." 

In  addition  to  the  character  of  the  accident  there  are 
several  other  considerations  of  importance  in  determining 
the  causation  of  the  traumatic  neuroses. 

Among  the  factors  active  in  the  production  of  general 
nervous  diseases,  an  important  place  is  occupied  by  predis- 
position, either  hereditary,  or  acquired  through  excesses  of 
any  kind.  In  neurasthenia  and  hysteria,  originating  from 
causes  other  than  trauma,  it  may  oftea  be  discovered  that 
previously  to  the  appearance  of  symptoms  the  resisting 
powers  of  the  nervous  system  had  become  enfeebled  through 
various  causes.  When  these  disorders  result  from  traumatic 
influences,  predisposition  to  nervous  disease,  either  heredi- 
tary or  acquired,  is  often  difficult  to  prove.  Traumatic  neu- 
rasthenia frequently  appears  in  persons  previously  healthy 
and  active,  and  in  cases  which  develop  hysteria  after  trauma 
it  is  often  impossible  to  discover  any  predisposition.  The 
question  of  predisposition  is,  however,  very  cursorily  treated 
in  many  reported  cases  of  this  character,  although  it  is  of 
the  highest  importance,  both  for  scientific  proofs  and  medico- 
legal purposes,  to  know  whether  organic  disease  or  an  en- 
feebled nervous  system  had  pre-existed.  It  should  make  a 
great  difference  in  a  verdict  if  an  injury  had  merely  caused 


212  FUNCTIONAL   EFFECTS   OF    INJURY. 

an  outbreak   in   symptoms  which   had   previously  existed, 
though  latent. 

Occupation  and  mode  of  life  exert  a  certain  influence  on 
the  occurrence  of  these  disorders.  Railway  employees, 
with  the  exception  of  locomotive  engineers  and  railway 
postal  clerks,  are  less  prone  than  passengers  to  develop 
hysteria  or  neurasthenia  after  accidents.  This  is  explained 
in  part  by  the  fact  that  the  employee,  having  become  more 
or  less  accustomed  to  the  ordinary  mishaps  incident  upon 
railway  travel,  can  bear  with  a  certain  degree  of  composure 
any  accident  in  which  he  is  not  severely  injured.  Also, 
when  an  employee  is  slightly  injured,  his  one  thought  is  to 
get  well  and  to  return  to  work  as  soon  as  possible.  For 
obvious  reasons  it  is  bad  policy  for  him  to  bring  suit  against 
the  company — a  limitation  which  acts  to  his  advantage,  for 
by  means  of  it  his  convalescence  is  not  delayed  by  the  anxi- 
ety and  vexations  which  commonly  attend  suits  for  dam- 
ages. Engineers,  as  distinguished  from  other  railway  em- 
ployees, do  not  share  in  the  comparative  immunity  from 
functional  nervous  disorders— an  exception  which  may  be 
in  part  explained  by  the  constant  nervous  strain  to  which 
their  responsibility  exposes  them. 

Railway  postal  clerks  are  frequently  victims  of  neuras- 
thenia. The  character  of  their  work  demands  that  they  be 
on  their  feet,  subject  to  the  constant  vibration,  swaying,  and 
jolting  of  the  rapidly  moving  train.  At  the  same  time,  the 
sorting  of  the  mail  requires  close  attention  and  concentrated 
mental  effort.  They  are,  consequently,  exposed  to  the  two 
most  fertile  causes  of  nervous  exhaustion. 

Contrary  to  the  generally  received  impression,  the  trau- 
matic neuroses  are  relatively  more  frequent  among  the 
poorer  classes.  As  a  reason  for  this  it  may  be  urged  that 
laboring  men  are  more  constantly  exposed  to  injury.  But, 
aside  from  this  unquestionable  fact,  it  seems  as  though  there 
were  something  in  the  mode  of  life  of  the  poorer  classes 


ETIOLOGY   OF   THE   TRAUMATIC   NEUROSES.  213 

which  rendered  them  particularly  susceptible  to  evil  results 
from  slight  traumatisms.  Perhaps  faulty  hygiene  furnishes 
the  predisposition,  of  which  the  existence  is  so  often  hard 
to  prove.  Men  are  more  frequently  affected  than  women,  a 
difference  which  can  be  explained  by  the  very  much  greater 
frequency  with  which  men  are  exposed  to  accidents  of  all 
kinds. 

T\\Q,  physical  co7tdition  of  the  person  at  the  time  of  the  ac- 
cident exerts  a  very  important  influence.  The  fact  is  well 
established  that  those  who  are  asleep,  or  under  the  influ- 
ence of  liquor,  experience  the  fewest  serious  results,  both 
physical  and  mental,  from  railway  and  allied  accidents.  On 
the  other  hand,  persons  suffering  from  chronic  disease  of  any 
kind,  and  particularly  disease  of  the  nervous  system,  are 
especially  susceptible  to  bad  effects  from  traumatism.  The 
original  disease  may  be  made  worse,  or  to  it  may  be  added 
symptoms  of  subjective  and  functional  character. 

Thus  in  an  unpublished  case  of  Peterson's,  which  he  kindly 
permits  me  to  quote,  a  lady  had  suffered  for  some  time  from  amyo- 
trophic lateral  sclerosis,  although  the  disease  had  only  annoyed 
her  by  interfering  with  the  finer  movements  of  the  hands.  One 
day,  while  sitting  in  a  restaurant,  she  was  struck  on  the  head  by  a 
revolving  fan,  which  had  become  detached  from  its  support  on 
the  ceiling.  As  a  result  of  this  there  supervened  a  condition  of 
extreme  nervousness,  irritability,  sleeplessness,  and  despondency 
— symptoms  previously  absent.  Also  tremor,  of  which  she  had 
never  complained  before,  became  very  marked  after  any  exertion 
or  fatigue. 

The    influence  of   suggestion   by  physicians   is   frequently 

traceable  in  the  causation   both  of  traumatic  neurasthenia 

and  of  traumatic  hysteria.    In  many  cases  it  seems  as  though 

these  disorders  owe  their  appearance,  in  large  part  at  least, 

to  the  fact  that  the  patients  have  been  told  by  physicians 

that  they  may  some  day  have  trouble  with  the  spinal  cord 

as  a  result  of  the  accident.     The  examples  of  the  bad  effects 

of  such  ill-advised  statements  are  numerous. 
15 


214  FUNCTIONAL   EFFECTS   OF   INJURY. 

Thus,  a  gentleman  was  slightly  jarred  by  the  sudden  stopping 
of  a  sleeping-car,  but  was  not  thrown  from  his  berth  and  felt  no 
immediate  ill  effects  of  the  mishap.  On  general  principles,  how- 
ever, the  next  morning  he  consulted  a  physician,  who  told  him 
that  his  spine  had  been  concussed  and  that  he  might  eventually 
have  serious  symptoms  as  a  result.  A  few  days  afterward  the 
patient  began  to  have  pain  in  the  back,  and  finally  became  a  con- 
firmed neurasthenic. 

Similarly,  a  park  policeman  was  thrown  from  the  back 
platform  of  a  horse-car,  striking  upon  the  pavement  with  his  face. 
He  thought  his  jaw  was  broken,  and  immediately  sought  medi- 
cal advice.  The  doctor  said  that  there  was  no  serious  injury 
about  the  head,  but  that  he  feared  trouble  from  the  spinal 
cord.  A  few  months  after  this  the  patient  came  to  the  Van- 
derbilt  Clinic,  presenting  a  pronounced  picture  of  traumatic 
hysteria. 

Intimately  allied  with  suggestion  as  a  causative  factor  of 
the  traumatic  neuroses,  and  by  some  considered  the  most 
important  of  all,  is  the  question  of  litigation.  In  how  far 
and  in  what  way  the  hope  of  compensation  for  personal  in- 
juries received  in  accidents  influences  the  development  of 
functional  nervous  symptoms  will  be  considered  in  succeed- 
ing pages.  In  speaking  here  of  aetiology,  it  is  sufficient  to 
say  that  there  is  a  far  greater  probability  that  functional 
nervous  disturbances  will  appear,  or,  if  they  have  already 
appeared,  that  they  will  be  made  worse,  in  any  case  which 
becomes  the  subject  of  medico-legal  inquiry.  Upon  this 
point  all  authorities  agree.  There  are  still  many  differences 
of  opinion  in  regard  to  the  pathology,  symptomatology,  and 
prognosis  of  the  traumatic  neuroses,  but  the  belief  in  litiga- 
tion as  a  very  potent  causative  factor  is  universal.  It  sur- 
rounds the  patient  with  the  influences  from  which  he  should 
be  free,  and  prevents  him  from  pursuing  the  course  of  treat- 
ment best  suited  to  permit  a  return  of  health  and  of  self- 
control.  It  is  the  physician's  duty  to  do  all  in  his  power  to 
favor  an  adjustment  of  claim,  rather  than  have  his  patient 
run  the  risk  of  becoming  a  chronic  invalid  through  the  vexa- 


SYMPTOMS   OF   THE    TRAUMATIC   NEUROSES. 


215 


tions  and  annoyances  which  are  invariably  associated  with 
suits  for  damages. 

Symptoms. — The  symptoms  of  the  traumatic  neuroses 
are  essentially  those  of  traumatic  neurasthenia  and  traumatic 
hysteria.  Inasmuch,  however,  as  these  two  disorders  often 
occur  together  in  accident  cases,  and  since  there  has  been  so 
much  discussion  relative  to  the  clinical  value  of  their  mani- 
festations, it  will  be  necessary  to  make  some  preliminary 
observations  on  the  general  character  of  the  symptoms,  al- 
though they  will  be  fully  described  in  later  chapters.  Many 
of  them  are  purely  subjective.  In  private  practice,  when 
the  physician  has  to  deal  with  subjective  symptoms,  he  is 
usually  safe  in  believing  that  they  really  are  causes  of  annoy- 
ance or  suffering  to  the  patient,  although  it  may  be  evident 
that  they  are  to  a  certain  extent  exaggerated.  When  the 
question  of  litigation  enters,  however,  the  case  becomes  en- 
tirely different ;  then,  instead  of  looking  for  the  harmless 
exaggeration  of  chronic  invalidism,  the  examiner  must  be  on 
his  guard  against  malingering.  To  insure  correct  results 
from  the  examination  of  litigation  cases,  it  is  necessary  that 
the  physician  be  cognizant  of  fraud,  familiar  with  the  meth- 
ods of  diagnosis  of  nervous  disease,  and  aware  that  the  func- 
tional disorders  may  be  serious  or  incurable  affections.  The 
examiner,  whether  he  be  an  expert  called  by  a  claimant,  or 
be  employed  by  a  corporation,  should  undertake  the  exami- 
nation without  prejudice  and  without  bias.  His  position  is 
always  delicate  and  often  difficult.  It  would  be  superfluous 
to  dwell  here  upon  the  moral  duties  of  an  examiner  in  litiga- 
tion cases.  Thaj;  is  a  question  in  ethics  rather  than  in  medi- 
cine.  The  physician  owes  it  to  his  client  to  exert  every  effort 
in  his  behalf.  He  owes  it  to  himself  to  give  an  opinion  based 
solely  upon  his  own  convictions.  By  whomsoever  employed, 
he  will  rarely  err  if  he  keeps  constantly  in  mind  that  his  func- 
tion is  scientific,  and  that  he  is  not  to  be  influenced  by  the  ef- 
fect his  opinion  will  have  upon  the  financial  aspect  of  the  case. 


2i6  FUNCTIONAL   EFFECTS   OF    INJURY. 

It  is  often  impossible  to  decide  from  a  single  examina- 
tion what  the  merits  of  the  case  really  are,  and  in  doubtful 
cases  an  opinion  should  not  be  given  until  after  several  have 
been  made.  In  general  practice  the  physician  often  finds 
himself  unable  to  determine  the  exact  nature  of  a  disease 
until  he  has  observed  it  during  a  considerable  period  of 
time.  How,  then,  in  any  accident  case,  in  which  the  symp- 
toms are  almost  entirely  subjective,  and  in  which  exist  the 
strongest  motives  for  exaggeration  or  deceit,  can  he  hope  to 
be  always  correct  in  diagnosis  and  prognosis  from  examin- 
ing the  patient  once  only  ?  In  Germany,  laboring  men  who 
are  the  victims  of  accidents  can  be  placed  in  the  hospital 
until  the  exact  nature  of  the  disorder  becomes  plain.  Such 
a  procedure  is  impossible  in  America.  With  us  only  those 
persons  go  to  the  hospital  who  are  seriously  injured,  and 
about  whose  injuries  there  could  be  no  question  of  doubt. 
The  others  must,  for  the  greater  portion  of  the  time,  be  free 
from  medical  observation.  This  fact  should  render  the  phy- 
sician  cautious  about  too  unreservedly  accepting  the  patient's 
statements,  or  about  placing  too  high  a  value  upon  such 
symptoms  as  are  purely  subjective  in  character.  The  his- 
tory of  how  injuries  were  received,  or  the  accounts  of  phys- 
ical conditions,  are  often  unreliable  when  told  by  persons 
unfamiliar  with  the  significance  of  symptoms  or  with  the 
general  workings  of  pathology.  To  a  certain  extent  in  gen- 
eral  medical  cases,  and  to  a  greater  extent  in  functional  nerv- 
ous troubles,  when  there  is  no  thought  of  litigation,  the  ph}^- 
sician  must  be  guided  by  the  results  of  his  own  examination 
rather  than  by  the  description  of  suffering^  and  discomfort 
given  by  the  patient.  In  cases  in  which  the  strongest  mo- 
tives for  exaggeration  and  deceit  are  present,  how  much 
more  conservative  must  he  be  about  too  fully  accepting 
statements  of  personal  ill  health  which  permit  of  no  ob- 
jective proof ! 

The  history  may  be  unreliable  even   when  the  patient 


SYMPTOMS   OF    THE   TRAUMATIC   NEUROSES. 


217 


believes  it  to  be  true.  By  constantly  rehearsing  in  his  mind 
the  details  of  the  accident  as  he  remembers  them,  or  as  they 
have  been  told  him  by  witnesses,  by  the  sympathetic  in- 
quiries and  solicitations  of  friends  or  interested  persons, 
the  patient  may  come  to  believe  that  he  knows  for  him- 
self what  has  in  reality  been  told  him  or  suggested  to  him 
by  others. 

It  is,  of  course,  not  meant  that  the  examiner  should  neces- 
sarily disbelieve  everything  that  a  claimant  tells  him.  But 
the  history  of  the  traumatic  neuroses  has  shown,  and  the 
nature  of  the  cases  demands,  that  the  statements  of  patients 
in  litigation  cases  should  be  subjected  to  some  corroborative 
proof  before  they  are  unreservedly  accepted  as  true.  The 
proof  of  the  reality  of  the  painful  sensations  from  which  the 
patient  says  he  suffers  may  often  be  found  in  his  manner  and 
general  bearing.  His  whole  appearance  may  indicate  ill 
health,  although  there  is  no  one  objective  symptom  to  prove 
its  existence.  It  is  then  that  the  physician  must  be  guided 
by  his  own  experience  in  nervous  disease.  But  when  there 
are  no  physical  traces  left  by  the  suffering  through  which  a 
claimant  says  he  has  gone,  or  to  which  he  asserts  he  is  still 
subject,  there  is  no  way  in  which  it  may  be  decided  as  to 
the  unreality  of  the  symptoms,  except  in  so  far  as  repeated 
medical  examinations  may  show  their  existence  to  be  im- 
probable, or  in  so  far  as  information  from  outside  sources 
may  prove  that  the  claimant  only  conducts  himself  like  a 
sick  man  when  he  is  being  watched.  Thus  must  be  deter- 
mined the  truth  concerning  such  symptoms  as  sleeplessness, 
spontaneous  pain,  nervousness,  lack  of  interest,  and  general 
fatigue.  Some  of  the  symptoms  commonly  called  objective 
are  also,  in  large  part  at  least,  subjective. 

Excitability  of  the  heart  and  rapid  pulse,  although  ob- 
jective signs,  are  not  in  themselves  necessarily  evidences  of 
disease. 

Palpitation  of  the  heart  is  particularly  frequent  in  per- 


21 8  FUNCTIONAL   EFFECTS   OF   INJURY. 

sons  who  use  to  excess  tea,  alcohol,  tobacco,  or  other  stimu- 
lants. 

In  most  people  the  heart  becomes  more  rapid  at  the 
time  of  a  medical  examination,  and  in  those  of  a  nervous 
temperament  the  heart  action  may  become  tumultuous  from 
very  slight  excitement.  The  same  observation  holds  good 
for  anomalies  of  respiration. 

Ancesthesia  is  the  symptom  about  the  diagnostic  value  of 
which  there  has  been  the  greatest  contention. 

It  has  been  urged  against  it  that  the  symptom  is  subject- 
ive, inasmuch  as,  with  the  exception  of  tests  which  are  pain- 
ful, the  physician  gains  his  information  from  the  patient, 
who,  through  inattention  or  through  the  influence  of  sugges- 
tion, or  when  actuated  by  ulterior  motives,  may  make  an- 
swers which  are  not  true,  and  thus  be  credited  with  symp- 
toms which  do  not  exist.  Yet,  although  anaesthesia  is  a 
subjective  symptom  in  the  sense  that  the  co-operation  of  the 
patient  is  often  necessary  for  the  establishment  of  its  exist- 
ence, it  is  converted  into  an  objective  symptom  when  the 
replies  of  the  person  under  examination  show  it  to  be  in 
accord  with  the  other  disease  evidences  which  may  be  pres- 
ent, and  in  agreement  with  the  loss  of  sensibility  recognized 
as  characteristic  of  definite  clinical  types.  There  is  no  ques- 
tion as  to  the  objectivity  of  anaesthesia  as  observed  in  spinal- 
cord  lesions  or  in  classical  cases  of  hysteria.  When,  how- 
ever, the  loss  of  sensibility  is  slight,  occurring  in  small  areas 
with  indefinite  boundary  lines,  or  in  the  form  of  a  general 
blunting  of  the  sense  of  touch  or  of  pain,  its  diagnostic  value 
is  not  great  and  can  easily  be  overestimated. 

Acuteness  of  cutaneous  sensibility  is  subject  to  wide 
variations  which,  clinically  at  least,  must  be  regarded  as 
within  normal  limits.  It  varies  with  age,  sex,  and  race, 
with  different  individuals  under  similar  circumstances,  and 
with  the  same  individual  under  the  changing  effects  of 
weather,  time  of  day,  fatigue,  and  similar  temporary  condi- 


SYMPTOMS   OF    THE    TRAUMATIC   NEUROSES.  2IQ 

tions.  Certain  diseases,  such  as  general  paresis  and  chronic 
intoxications,  notably  alcoholism,  in  which  pronounced  an- 
aesthesia is  not  usually  present,  are  often  accompanied  by  a 
certain  degree  of  blunting  of  sensibility.  When  due  allow- 
ance is  made  for  these  variations  angesthesia  remains  as  a 
symptom  of  positive  and  often  of  pathognomonic  usefulness. 
The  physician  who  is  familiar  with  the  facts  will  appreciate 
the  appropriate  value  of  the  symptom,  and  will  not  be  apt 
to  ascribe  to  slight  impairment  of  sensibility  an  unwarranted 
diagnostic  importance. 

Pain  or  hypercBsthesia  is  subjective,  except  in  so  far  as  it 
leaves  unmistakable  evidences  in  disturbances  of  nutrition. 
A  test  usually  considered  as  of  considerable  value  for  the 
determination  of  the  genuineness  of  pain  and  for  converting 
it  into  an  objective  symptom  has  been  named,  after  its  origi- 
nal describer,  Mannkopff,  although  its  applicability  in  the 
traumatic  neuroses  was  first  pointed  out  by  Rumpf.  It  con- 
sists in  observing  the  pulse  rate  before,  after,  and  during 
pressure  upon  an  area  alleged  to  be  painful.  If  the  pulse 
becomes  more  rapid  while  the  pressure  is  being  made,  it  is 
supposed  to  be  proof  that  the  pain  is  real  and  has  reflexly 
caused  the  heart  to  beat  more  rapidly.  The  application  of 
the  test  is  illustrated  by  Rumpf  in  the  following  case  : 

A  man,  thirty-three  years  of  age,  fell  from  a  roof.  After  the 
various  early  symptoms  of  injury  had  disappeared  the  patient 
still  complained  of  great  weakness  and  pain  in  the  head,  back, 
and  left  breast,  which  was  much  increased  by  any  contact.  The 
pain  was  entirely  subjective,  but  was  converted  into  an  objective 
symptom  by  the  Mannkopff  test.  To  avoid  confusing  the  in- 
crease of  the  pulse  rate,  due  to  fear  or  other  psychic  influences, 
with  the  increase  caused  by  the  perception  of  real  pain,  the  pulse 
was  first  counted  with  the  patient  in  the  recumbent  posture  with- 
out any  pressure  being  applied  to  the  painful  areas.  The  rate 
was:  In  the  first  quarter  of  a  minute,  20;  in  the  third  quarter  of 
a  minute,  24;  in  the  fifth  quarter  of  a  minute,  29;  in  the  seventh 
quarter  of  a  minute,  26  ;  in  the  ninth  quarter  of  a  minute,  26  ;  in 
the  eleventh  quarter  of  a  minute,  25.     Then  firm  pressure  was  ap- 


220  FUNCTIONAL   EFFECTS   OF    INJURY. 

plied  to  the  alleged  painful  area  in  the  back,  and  the  pulse  at  once 
increased  to  33  beats  in  the  first  quarter.  On  removing  the  pres- 
sure it  sank  again  as  follows  :  In  the  first  quarter  of  a  minute,  32  ;. 
in  the  third  quarter  of  a  minute,  30 ;  in  the  fifth  quarter  of  a  min- 
ute, 28,  in  the  seventh  quarter  of  a  minute,  27;  in  the  ninth 
quarter  of  a  minute,  25.  In  addition  to  an  increase  in  rate,  the 
pulse  became  smaller  and  at  times  irregular. 

Rumpf  regarded  the  Mannkopff  test  as  of  great  value  in 
the  detection  of  simulation ;  but  observations  made  by- 
Strauss,  in  which  the  pulse  waves  were  carefully  recorded 
by  means  of  the  sphygmograph,  have  shown  that  in  many 
cases  of  unquestioned  pain,  pressure  over  the  painful  areas- 
causes  no  increase  in  the  heart's  action  ;  so  that  Strauss's 
conclusions,  which  accord,  I  think,  with  those  of  most  clini- 
cians, is  that  the  Mannkopff  symptom  is  not  constant  even 
in  cases  in  which  there  is  no  reason  to  doubt  the  real  exist-^ 
ence  of  pain  or  hyperesthesia.  If  the  symptom  is  present, 
as  it  often  is  in  traumatic  lumbago,  or  as  it  may  be  in  hys- 
teria, it  is  a  valuable  aid  in  diagnosis.  But  if  it  is  absent,  we 
are  by  no  means  justified  in  concluding  for  that  reason  that 
the  pain  or  hypergesthesia  is  assumed.  In  making  the  test 
the  pulse  should  be  carefully  counted  for  some  little  time 
before  exerting  the  pressure,  in  order  to  eliminate  as  far  as 
possible  any  acceleration  which  may  be  due  to  psychic  influ- 
ences.    This  test  may  be  extremely  painful. 

The  visual  disturbances  of  the  traumatic  neuroses  have 
been  the  subject  of  much  controversy.  There  is  no  reason 
.  to  doubt  that  in  neurasthenia  there  is  commonly  an  asthe- 
nopia, which  prevents  any  long-continued  use  of  the  eyes, 
and  that  some  of  the  visual  anomalies  of  hysteria,  although 
very  difficult  to  explain,  are  pathognomonic  of  that  disease. 

The  chief  contention  among  neurologists  has  been  in 
regard  to  the  diagnostic  value  of  the  results  of  perimetric 
examinations.  The  two  conditions  most  commonly  observed 
in   such   examination   of   cases   of   the  traumatic  neuroses. 


SYMPTOMS   OF   THE   TRAUMATIC   NEUROSES.  221 

have  been  the  concentric  contraction,  without  structural 
disorder  of  the  eye,  and  the  shifting  or  fatigue  contraction 
of  the  visual  fields  (see  Chapter  II).  The  first  of  these  con- 
ditions was  originally  described  by  von  Graefe  and  the  sec- 
ond by  Forster. 

In  regard  to  both  of  them  arises,  as  it  must  arise  in 
regard  to  any  functional  symptom,  the  question,  Do  they 
occur  in  normal  individuals,  and  do  they  occur  in  other 
diseases  in  a  way  to  impair  their  diagnostic  value  for  the 
traumatic  neuroses  ? 

The  recent  investigations  of  Koenig  indicate  very  posi- 
tively that  concentric  limitation  of  the  visual  fields  is  not 
found  in  persons  with  normal  nervous  systems.  From  the 
examination  of  two  hundred  and  sixteen  non-nervous  cases 
and  of  ten  pathological  cases,  Koenig  concludes  that  it  does 
not  occur  in  healthy  persons,  that  it  may  be  the  only  symp- 
tom of  hysteria,  and  that,  when  constant,  it  is  typical  of  hys- 
teria, even  when  the  limitation  is  only  slight  in  degree. 

This  ocular  condition  is  observed  in  many  of  the  disor- 
ders of  the  nervous  system,  of  which  the  most  prominent 
are  tabes,  dementia  paralytica,  epilepsy,  trigeminal  neural- 
gia, and  alcoholism.  But  occurring  in  this  way,  even  if  the 
routine  examination  of  the  eye  fails  to  disclose  any  other 
visual  defects,  the  associated  symptoms  will  prevent  the 
contraction  of  the  visual  field  being  ascribed  to  hysteria 
alone.  A  consideration  of  these  facts,  together  with  the 
great  improbability  of  the  simulation  of  the  condition,  seems 
to  justify  the  acceptance  of  contraction  of  the  visual  field, 
when  there  are  no  morbid  alterations  of  eye  structure,  and 
when  symptoms  of  other  forms  of  functional  or  organic  dis- 
ease are  absent,  as  a  pathognomonic  symptom  of  hysteria. 

The  significance  of  the  shifting  type  of  contraction  is  not 
so  well  established.  Peters  has  found  it  present  in  many 
persons  presumably  healthy.  Koenig,  however,  and  still 
more  recently  Miiller,  incline  to  the  view  that,  if  at  all  pro- 


222  FUNCTIONAL   EFFECTS   OF   INJURY. 

nounced,  this  symptom  is  certainly  indicative  of  retinal  fa- 
tigue ;  and  that  although  it  may  occur  in  healthy  men,  in 
them  it  is  less  constant  and  less  pronounced.  As  Miiller 
says,  when  it  is  constantly  present  at  repeated  examinations 
in  persons  supposedly  healthy,  it  is  time  to  look  for  nervous 
symptoms. 

The  te?idon  reflexes,  and  especially  the  hiee-jerk,  become 
the  subject  of  discussion  in  most  accident  cases.  Loss  of 
knee-jerk  does  not  occur  as  the  result  of  functional  disease. 
Exaggeration,  on  the  other  hand,  is  the  rule.  Unless  asso- 
ciated with  other  symptoms,  slight  exaggeration  can  not  be 
regarded  as  of  any  particular  pathological  significance : 
when  associated  with  ankle  clonus,  it  usually,  though  not 
invariably,  indicates  organic  disease ;  when  associated  with 
other  symptoms,  it  lends  confirmatory  evidence  as  to  the  ex- 
istence of  morbid  functional  states. 

Vomiting  or  spitting  up  of  blood-stained  fluid  immediately 
after  the  accident,  occurs  in  a  certain  proportion  of  the 
cases.  While  alarming  in  appearance,  this  symptom  has  no 
particular  significance  unless  it  is  the  result  of  injury  to  the 
thoracic  contents  or  to  pre-existing  disease  of  the  lungs.  It 
is  observed  in  neurasthenia,  but  more  commonl}^  in  hysteria. 
The  discharge  comes  from  the  mucous  membrane  of  the 
mouth  and  throat,  and,  as  Striimpell  has  shown,  is  character- 
ized by  the  small  number  of  red  blood-cells  and  by  the  free 
mixture  of  mucous  epithelium  and  bacteria  which  are  col- 
lected in  the  buccal  and  pharyngeal  mucous  membrane. 

Glycosuria,  as  a  result  of  injuries  to  the  nervous  system, 
is  a  condition  about  which  more  information  is  desirable. 
The  most  that  can  be  said  of  it  is  that,  while  it  may  occur  as 
the  result  of  injuries  to  the  brain  and  medulla,  temporary 
glycosuria  is  occasionally  found  after  injuries  whose  chief 
results  are  functional. 

The  other  symptoms  of  the  traumatic  neuroses  will  be 
so  fully  described  in  succeeding  pages  that  they  require  no 


SYMPTOMS   OF    THE    TRAUMATIC   NEUROSES.  223 

mention  here.  It  is  to  be  remembered,  however,  that  it  is 
not  by  the  consideration  of  any  one  symptom  that  a  com- 
plete comprehension  of  any  case  of  functional  nervous  dis- 
ease following  an  accident  is  to  be  obtained.  The  case 
must  be  looked  at  in  its  clinical  entirety.  Attention  must 
be  given  to  the  kind  of  accident  and  the  extent  of  physical 
injury  as  well  as  for  motives  for  simulation  or  exaggera- 
tion. It  is  not  sufficient  to  observe  objective  symptoms 
without  inquiring  whether  they  could  not  have  antedated 
the  accident.  It  is  not  possible  to  form  a  conclusion  from 
one  subjective  symptom. 

By  refusing  to  express  an  opinion  without  having  looked 
at  the  case  in  every  aspect  the  physician  will  rarely  find 
himself  in  error, 

Bibliography. 

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Booth,  Critical  Digests  in  Sajous's  A7m.  of  the  Utiiv.  Med.  Sci., 
1892,  1893,  1894. 

Bruns,  Critical  Digests  in  Schmidt's  Jah?'bikher,  ccxx,  p.  142  ; 
ccxxi,p.  210;  ccxxx,  p.  81;  ccxxxi,  p.  21;  ccxxxiv,  p.  25  ;  ccxxxviii 
p.  73;  ccxlii,  p.  191  ;  cclv,  8. 

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1889. 

Crocq,  fils,  Etude  pathogenique  et  clinique  des  nevroses  trau- 
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Dana,  Concussion  of  the  Spine  and  its  Relation  to  Neurasthe- 
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224  FUNCTIONAL   EFFECTS   OF   INJURY. 

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Knapp,  Accidents  from  the  Electric  Current.  Bost.  Med.  and 
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BIBLIOGRAPHY   OF    THE    TRAUMATIC    NEUROSES. 


225 


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CHAPTER   II. 

TRAUMATIC   NEURASTHENIA. 

Neurasthenia  is  a  condition  of  irritable  weakness  of 
the  nervous  centers,  as  a  result  of  which  they  become  less 
tolerant  of  external  impressions  and  of  the  effects  of  fa- 
tigue. It  is  a  condition  rather  than  a  disease  ;  but,  although 
it  most  commonly  occurs  without  there  being  any  structural 
lesion  of  important  organs,  its  clinical  picture  is  so  typical 
and  its  symptoms  are  so  well  marked  that  the  disorder, 
when  pronounced,  is  usually  spoken  of  as  though  it  were  a 
disease.  The  clinical  manifestations  of  neurasthenia  are  the 
results  of  a  loss  of  potential  nervous  energy.  From  what- 
ever cause  it  may  have  been  induced,  the  patient  presents 
the  symptoms  of  a  diminished  power  of  resistance  to  the  in- 
fluences of  fatigue  and  a  hyperexcitability  of  the  nervous 
centers.  He  is  quickly  exhausted  by  mental  and  physical 
exertion,  and  reacts  too  strongly  to  all  forms  of  peripheral 
irritation.  The  neurasthenic  is  incapable  of  prolonged  men- 
tal or  physical  work,  and  such  efforts  are  quickly  followed 
by  confusion  and  fatigue.  All  the  receptive  centers  are  hy- 
persensitive, so  that  there  is  a  morbid  increase  of  response 
to  all  peripheral  stimuli,  and  the  individual  becomes  intoler- 
ant of  such  shght  irritations  as  pass  in  health,  if  not  unob- 
served, at  least  without  being  followed  by  sensations  which 
are  painful. 

Neurasthenia  may  exist  in  varying  degrees.  Temporary 
nervous  exhaustion  naturally  follows  excessive  work  of  any 

kind.     Any  one  who  has  become  over-fatigued  by  mental 

226 


TRAUMATIC   NEURASTHENIA. 


227 


strain  or  by  excessive  work,  will  present  most  of  the  symp- 
toms of  neurasthenia.  But  in  the  majority  of  persons,  the 
evidences  of  exhaustion  which  ma}'-  be  present  at  night 
after  a  hard  day's  work,  have  vanished  in  the  morning- 
when  sleep  has  permitted  a  restoration  of  vigor  to  the  nerv- 
ous system.  When  the  overwork  is  continued  for  too  long 
a  time,  however,  or  when  the  rest  is  inadequate,  the  symp- 
toms, which  at  first  were  temporary,  may  tend  to  become 
more  and  more  permanent ;  and  the  tired  man  or  woman, 
instead  of  presenting  such  effects  of  overwork  as  may  be 
easily  repaired,  may  become  a  clinical  type  of  pronounced 
neurasthenia — a  condition  which  requires  more  than  ordi- 
nary rest  for  its  cure.  Under  the  name  of  nervous  prostra- 
tion, neurasthenia  has  come  to  be  a  generally  familiar  affec- 
tion. It  is  commonly  spoken  of  as  a  disorder  which  is 
directly  amenable  to  the  will,  in  that  a  person  suffering  from 
it  might  be  well  if  he  could  bring  himself  to  believe  that  he 
were  not  ill.  This  is  true  in  part  only.  The  nervous  ex- 
haustion has  to  a  great  extent  robbed  the  patient  of  the 
ability  to  control  his  own  mental  processes ;  and  to  restore 
the  will  power  there  must  be  a  return  of  energy  to  the  nerv- 
ous centers,  by  the  exhaustion  of  which  it  has  been  lost. 

i^tiology. — Since  the  description  of  neurasthenia  by 
Beard,  the  disorder  has  been  generally  recognized.  It  may 
complicate  any  of  the  chronic  diseases,  it  frequently  results 
from  overwork,  anxiety,  and  excess  of  any  kind,  and  in  some 
cases  it  develops  without  apparent  cause.  The  fact  that  it 
may  develop  primarily  as  a  result  of  injury  and  shock  has 
only  been  recognized  in  recent  years.  When  occurring  in 
this  way  it  is  called  traumatic  neurasthenia,  and  differs  only 
in  slight  particulars  from  neurasthenia  due  to  other  causes. 
The  back  injury  and  the  effects  of  litigation  have  given  cer- 
tain peculiarities  to  traumatic  neurasthenia,  but  the  under- 
lying conditions  and  essential  symptoms  are  the  same  in  all 
varieties  of  the  disorder. 


228  FUNCTIONAL   EFFECTS   OF   INJURY. 

Traumatic  neurasthenia  is  by  far  the  most  frequent  func- 
tional nervous  affection  which  occurs  as  a  result  of  accident. 
Its  causation  has  already  been  described  in  a  general  way. 
The  disorder  is  infrequent  in  the  old  or  in  the  young,  most 
commonly  occurring  in  the  active  periods  of  life.  It  has 
been  reported  as  occurring  in  children.  Vibert  records  two 
cases  of  "  traumatic  neurosis "  observed  in  children  aged 
respectively  three  and  a  half  and  five  years.  From  Vibert's 
description,  these  cases  seem  to  present  the  symptoms  of 
psychic  epilepsy  rather  than  those  of  neurasthenia ;  and 
the  functional  nervous  disturbances  following  accidents, 
which  I  myself  have  observed  in  children,  have  been  sug- 
gestive of  a  more  profound  affection  of  the  nervous  system 
than  neurasthenia.  Men  are  much  more  frequently  affected 
than  women.  Nervous  predisposition,  although  demonstra- 
ble in  some  cases,  does  not  appear  to  be  an  essential  factor 
in  the  development  of  the  disorder. 

The  accident  is  the  most  important  causative  factor  of 
traumatic  neurasthenia.  The  fact  that  it  very  frequently  fol- 
lows accidents  on  railways  gained  for  it  the  original  name 
of  railway  spine. 

Although  it  also  frequently  follows  any  of  the  accidents 
in  which  the  factors  of  fright  and  physical  commotion  are 
prominent,  there  is  something  about  a  railway  accident 
which  seems  particularly  well  adapted  to  call  into  action  the 
peculiar  chain  of  nervous  symptoms  which  are  known  as 
neurasthenic. 

The  reasons  for  this  can  not  altogether  be  explained  by 
the  medico-legal  aspects  of  railway  accidents,  although  trau- 
matic neurasthenia  has  become  more  frequent  with  the  con- 
stant increase  in  litigation.  It  may  be  in  part  explained  by 
physical  reasons.  Railway  collisions  and  derailments  usu- 
ally put  unusual  strain  upon  the  back,  and  pain  in  the  back 
is  generally  the  first  and  most  constant  symptom  of  the  dis- 
order.    In  the  course  of  non-traumatic  neurasthenia,  also,  the 


TRAUMATIC   NEURASTHENIA. 


229 


backache  is  a  prominent  symptom.  It  may  be  that  a  rail- 
way accident,  in  causing  strain  of  the  spinal  ligaments  and 
muscles,  and  consequently  pain  in  the  back,  furnishes  at 
the  outset  one  of  the  most  characteristic  symptoms  of  neu- 
rasthenia, to  which  general  nervous  shock  and  subsequent 
events  add  others.  The  fact  remains  that  most  railway  ac- 
cidents do  cause  back  strain,  through  the  violent  shaking  of 
the  whole  body,  and  traumatic  neurasthenia  usually  begins 
with  pain  in  the  back.  In  severe  collisions  the  victim  may 
be  thrown  backward  and  forw^ard  many  times  before  the  car 
ultimately  comes  to  rest.  The  legs  or  the  trunk  may  be 
caught  and  jammed  between  the  seats  or  other  objects,  and 
the  free  portions  of  the  body  may  sustain  violent  wrenches 
.and  twists,  which  are  felt  chiefly  in  the  spine.  Even  when 
the  passenger  is  merely  thrown  from  his  seat  to  the  floor,  or 
pitched  against  the  seat  in  front  of  him,  the  suddenness  of 
the  force  and  the  involuntary  resistance  which  is  offered  by 
the  muscles  of  the  trunk  and  back  put  considerable  strain 
upon  the  spinal  ligaments  and  muscles.  The  sudden  stop- 
ping or  starting  of  a  train  may  cause  the  spine  to  be  con- 
siderably wrenched.  Thus  some  cases  of  back  strain  occur 
when  there  has  been  no  serious  accident.  In  addition  to 
the  local  injury,  railway  catastrophes  usually  cause  the  most 
severe  mental  shock  that  can  be  imagined.  An  association 
of  these  two  factors,  the  physical  and  the  psychical,  is  the 
commonest  cause  of  traumatic  neurasthenia. 

Can  shock  alone,  when  the  back  is  not  injured,  cause 
traumatic  neurasthenia  ?  Such  a  result  is  unusual.  If  a  per- 
son is  very  much  frightened  by  any  accident  he  may  in 
future  be  morbidly  nervous  about  re-exposing  himself  to 
that  especial  variety  of  danger.  A  victim  of  a  severe  rail- 
way collision  may  never  again  be  able  to  feel  at  ease  while 
on  the  railway,  although  he  may  never  have  been  physically 
injured    in  traveling.     It  is  a  fact  of   common    experience 

that  runaway  accidents,  even  when  no  injury  is  received, 
16 


230  FUNCTIONAL   EFFECTS   OF   INJURY. 

may  cause  a  timidity  about  driving  which  is  never  over- 
come. But  the  morbid  fears  that  result  from  accidents  in 
which  no  physical  injury  has  been  received  are,  in  the  ma- 
jority of  cases,  systematized,  and  relate  only  to  the  particu- 
lar form  of  accident  by  which  the  person  has  been  fright- 
ened. 

When  general  neurasthenic  symptoms  develop  from 
fright  alone,  it  is  probable,  in  most  cases  at  least,  that  the 
person  was  in  a  nervous  condition  at  the  time  of  the  acci- 
dent, or  that  some  injury  was  received  which  passed  unob- 
served. 

However,  when  the  nervous  shock  is  severe,  neuras- 
thenia sometimes  results,  although  the  physical  injury  be 
but  trifling.  Schaefer  relates  the  case  of  a  locomotive  engi- 
neer in  whom  the  fear  of  an  impending  collision  and  over- 
exertion in  stopping  the  train  produced  typical  symptoms. 
In  the  following  case  also  the  physical  element  must  have 
been  unimportant: 

A  Russian  Hebrew,  aged  thirty-nine,  came  to  the  Vanderbilt 
Clinic  on  June  3,  1896.  He  said  that,  until  the  preceding  May,, 
he  had  ahvays  been  healthy,  and  came  of  a  long-Hved  and  healthy 
family.  He  had  no  bad  habits,  was  married,  and  had  several 
healthy  children.  Denied  venereal  disease.  He  is  a  furrier  by 
trade.  It  is  not  probable,  however,  that  this  occupation  had  pre- 
disposed him,  by  chronic  mercurial  poisoning,  to  nervous  disease. 
Although  some  workers  in  furs  become  poisoned  by  inhahng 
the  mercury  with  which  furs  are  prepared,  such  a  result  only 
occurs  when  the  furs  are  heated  and  the  mercury  is  volatilized. 
Our  patient  had  been  exposed  to  no  such  danger,  and  denied, 
furthermore,  all  symptoms  of  hydrargyrism.  This  man  had  no 
motive  for  malingering.  He  has  never  had  any  thought  or  cause 
of  bringing  an  action  ;  he  is  a  member  of  no  lodge  or  society. 
When  not  at  work,  the  only  money  he  gets  is  drawn  from  what 
little  he  has  saved  or  what  is  earned  by  his  wife.  Since  an  acci- 
dent, which  must  have,  at  best,  been  attended  with  slight  physical 
commotion,  he  has  been  totally  unable  to  work.  I  saw  the  man 
in   February,    1897 — nearfy    one   year    after    the    accident — when 


TRAUMATIC    NEURASTHENIA. 


231 


he  told  the  following  story  and  presented  the  following  symp- 
toms: 

At  the  time  of  a  fire  at  Bleecker  Street  and  Broadway  he  was 
leaning  out  of  a  window  watching  the  disturbance.  His  head  and 
shoulders  were  out  of  the  window,  the  abdomen  resting  on  the 
window  sill  and  the  feet  on  the  floor. 

As  a  result  of  the  explosion  of  two  boilers  which  were  in  the 
burning  structure  opposite,  the  building  in  which  he  was  at  the 
time  was  jarred,  but  not  enough  to  break  any  glass  or  to  cause 
the  plastering  to  fall  from  the  walls.  The  man  was  very  much 
frightened,  and  he  felt  the  concussion  through  his  whole  body, 
but  he  was  not  dislodged  from  his  place.  Upon  getting  out  of 
the  window  frame,  he  fell  down,  but  quickly  picked  himself  up, 
and  was  busy  and  constantly  on  his  feet  for  the  rest  of  the  day. 
That  evening  he  went  to  bed,  and  stayed  there  for  two  weeks, 
feeling  weak  and  sick.  Soon  after  the  accident  the  patient  began 
to  have  pain  in  the  back,  and  has  had  it  ever  since.  There  was 
no  vomiting,  no  loss  of  sensation,  no  trouble  with  the  bowels  or 
rectum,  and  no  paralysis.  When  well  enough  to  leave  his  bed,  he 
tried  to  resume  work  again,  but  could  not  do  so  on  account  of 
the  trembling  of  the  fingers  and  the  pain  in  the  back. 

He  is  a  man  of  fairly  good  color,  but  has  the  anxious,  tired 
look  of  neurasthenia.  The  back  is  painful  in  its  whole  extent — 
from  the  cervical  to  the  lumbar  region.  Pressure  over  the  spinous 
processes  is  painful,  but  does  not  cause  the  heart  to  beat  more 
rapidly.  The  skin  over  the  whole  back  is  hypersensitive.  There 
are  no  evidences  of  organic  disease.  The  pupils  are  equal,  and 
react  readily  to  light.  The  optic  nerves  are  normal.  There  is 
a  slight  peripheral  limitation  of  the  visual  fields,  although  it  is 
difficult  of  determination.  There  is  nowhere  any  loss  of  sensa- 
tion. There  is  marked  tremor  of  the  face  and  in  the  hands,  con- 
stant, but  becoming  intensified  by  movement.  The  gait  is  slow 
and  uncertain  ;  the  knee-jerks  are  normal.  Appetite  good  ;  bowels 
regular.     During  his  illness  the  patient  has  lost  eighteen  pounds. 

In  this  case  there  was  some  physical  shaking,  although  it  must 
have  been  very  slight. 

In  some  rare  cases  there  seems  to  have  been  no  injury  at 
all.     Thus,  in  a  case  of  Page's : 

Neurasthenia  induced  by  fright.  Previous  ansmia.  A  lady, 
aged  twenty-four,  was  in   a  collision  which  took  place  at  night 


232  FUNCTIONAL   EFFECTS   OF   INJURY. 

without  the  slightest  warning.  The  baggage  fell  all  over  the  car- 
riage, and  her  husband  was  thrown  against  her,  but  she  herself 
was  neither  thrown  from  her  seat  nor  injured  in  any  single  part. 
As  soon  as  she  got  out  she  was  much  alarmed  at  seeing  a  carriage 
had  been  smashed  to  pieces,  and  then  she  watched  a  man  being 
rescued  from  the  debris  in  which  he  was  buried.  She  went  on  her 
journey,  and  the  next  day  felt,  to  use  her  own  words,  as  though 
she  had  passed  through  something  terrible ;  and  from  that  time 
onward  she  became  sleepless,  lost  her  appetite  and  strength,  suf- 
fered from  pain  in  the  back  of  the  head  and  at  several  spots  down 
the  spine,  and  was  quite  upset  by  any  attempts  at  household  work 
or  by  reading  and  writing.  Thinking  she  had  not  been  hurt,  her 
friends  urged  her  to  do  as  much  as  possible,  and  not  to  give  way, 
but  she  steadily  got  worse  rather  than  better ;  and  although  not 
in  the  least  hysterical,  it  was  not  until  proper  treatment  was  be- 
gun that  improvement  set  in.  The  case  was  complicated  by 
previous  dysmenorrhcea  and  anemia,  both  of  which  were  in- 
creased for  a  time  by  the  accident. 

These  cases  show  that  neurasthenia  may  result  from 
fright  when  the  physical  injury  has  been  insignificant.  It 
may,  on  the  other  hand,  follow  traumatisms  by  which  the 
patients  were  hurt  before  they  knew  that  they  were  in  dan- 
ger, and  so  escaped  the  fear  of  impending  injury.  These 
latter  cases  are  unusual,  for  shaking  of  the  whole  body  or 
injury  to  the  back  rarely  occurs  without  there  being  at  the 
same  time  some  terrifying  factors.  Few  participators  in 
railroad  accidents  escape  without  being  very  much  fright- 
ened ;  and  when  physical  injuries  are  received  in  any  way 
there  is  usually  a  period,  even  though  it  be  momentary,  of 
antecedent  alarm.  The  fright,  however,  is  often  trifling, 
as  when  caused  by  the  sudden  starting  of  a  train,  or  a  fall 
on  the  sidewalk  or  from  the  steps  of  a  carriage.  As  is  well 
known,  neurasthenia  may  follow  such  accidents. 

The  gravity  and  duration  of  the  symptoms  are  not  always 
in  proportion  to  the  severity  of  the  accident,  although  in 
general  the  more  severe  the  accident  the  more  rebellious 
will  be  the  resulting  neurosis. 


TRAUMATIC   NEURASTHENIA.  233 

As  neurasthenia  is  a  condition,  it  may  exist  in  very 
widely  varying  degrees  of  severity.  Many  persons  find 
themselves  after  an  accident  more  nervous  and  more  easily 
fatigued  than  they  were  before ;  but  the  impairment  of 
general  health  or  strength  may  be  so  slight  that  they  do  not 
complain,  and,  by  continuing  their  work  and  thus  keeping 
their  attention  away  from  their  own  troubles,  they  institute 
without  knowing  it  the  very  best  treatment  they  could  have. 
It  is  in  such  cases  as  these  that  the  anxiety  attendant  upon 
bringing  claims  or  litigation  may  render  very  serious  a  dis- 
order which  otherwise  would  have  been  trivial. 

Contrasted  with  the  frequency  with  which  neurasthenia 
remains  a  mild  affection,  is  the  fact  that  it  may  be  very 
severe,  and  render  its  victim  totally  incapacitated  for  work. 

In  recognizing  that  many  cases  are  transitory  and  easily 
repaired  by  proper  means,  sight  should  not  be  lost  of  the 
fact  that  the  disorder  may  be  intractable  or  even  incurable. 

Pathology. — Little  is  known  of  the  pathology  of  neuras- 
thenia. It  rarely  kills,  and  there  are  no  recorded  autopsies 
in  which  lesions  were  found  sufficiently  adequate  to  account 
for  the  neurasthenic  symptoms.  In  the  autopsies  which 
have  been  made  on  persons  who  died  during  the  course  of 
the  disorder  the  nervous  system  has  not  been  examined  with 
sufficient  care  to  discover  any  morbid  appearances  in  the 
ganglion  cells.  Hodge  and,  more  recently,  Lugaro  have 
shown,  however,  that  visible  alterations  of  form  and  struc- 
ture occur  in  the  ganglion  cells  of  animals  as  a  result  of 
fatigue.  And  since  fatigue  is  the  most  prominent  feature  in 
the  clinical  picture  of  neurasthenia,  it  is  to  be  inferred  that 
the  pathology  of  the  disorder  is  to  be  sought  for  in  the 
nutritional  disturbances  of  the  ganglion  cells.  It  would  be 
useless  to  speculate  here  as  to  how  these  changes  are 
brought  about,  or  what  their  essential  characteristics  are. 
It  is  enough  to  say  that  it  seems  probable  that,  to  explain 
the  disturbances  of  function,   there  are  structural  chano^es 


234  FUNCTIONAL   EFFECTS    OF   INJURY. 

which  may  eventually  be  seen  and  to  a  certain  extent  under- 
stood. But,  until  our  knowledge  regarding  the  pathology 
of  neurasthenia  is  more  exact  and  full,  it  must  continue  to 
be  classed  with  the  functional  diseases. 

Symptoms. — In  describing  the  symptoms  of  traumatic 
neurasthenia  it  must  be  understood  that  they  can  only  be 
regarded  as  belonging  to  that  category  when  they  can  not 
be  ascribed  to  organic  injury  of  the  nervous  system,  or  to 
functional  nervous  disease  more  serious  than  nervous  ex- 
haustion. 

The  mode  of  onset  of  the  symptoms  is  subject  to  many 
variations.  The  character  of  the  accident  and  the  influences 
by  which  the  patient  is  surrounded  both  before  and  after 
its  occurrence,  cause  great  differences  in  their  development. 
Persons  who  are  asleep  when  the  accident  occurs  are  spared 
much  of  the  shock  and  are  le'^s  liable  to  injury.  The  same 
is  true  for  persons  who  are  drunk.  The  two  conditions, 
sleep  and  intoxication,  render  the  development  of  neuras- 
thenia less  probable. 

Immediately  after  the  accident  there  may  be  consider- 
able prostration  and  shock.  The  patient  does  not  lose  con- 
sciousness, but  is  pale,  dizzy,  tremulous,  and  nauseated,  with 
cold  skin  and  rapid  pulse.  If  there  is  head  injury,  and 
sometimes  when  the  head  has  not  been  injured,  conscious- 
ness may  be  lost  for  a  variable  length  of  time.  If  the  body 
has  been  severely  bruised  or  lacerated,  the  earliest  symp- 
toms may  be  entirely  surgical.  The  latent  period,  includ- 
ing the  time  between  the  accident  and  the  first  appearance 
of  neurasthenic  symptoms,  varies  in  duration.  It  is  usually 
only  a  few  days,  though  it  may  last  for  several  weeks. 

The  ultimate  development  of  neurasthenic  symptoms  is 
to  a  great  extent  modified  by  those  influences  which  sur- 
round the  patient  immediately  after  the  accident.  Those  pa- 
tients do  best  who  can  put  themselves  immediately  in  a 
physician's  hands  without  thinking  too  much  of  claims  for 


TRAUMATIC   NEURASTHENIA. 


235 


damages.  Litigation  may  help  the  pocket,  but  does  so  at 
the  expense  of  health.  By  avoiding  it  the  appearance  of 
neurasthenic  symptoms  may  oftentimes  be  entirely  avoided. 

The  symptoms  of  traumatic  neurasthenia  are  various  and 
will  require  examination  in  detail.  When  the  disorder  dates 
from  the  time  of  a  railway  disaster,  the  story  is  often  some- 
what as  follows :  A  previously  healthy  man  while  riding  in 
a  railway  car  is  suddenly  startled  by  the  screech  of  the  loco- 
motive, and  almost  immediatel}^  afterward  experiences  a 
sudden  physical  shock,  is  thrown  violently  from  his  seat  to 
the  floor,  where  he  is  flung  backward  and  forward,  receiv- 
ing blows  upon  the  head  and  back.  Or  he  may  have  been 
caught  between  two  seats  and  his  back  twisted  or  wrenched. 
When  the  car  has  finally  come  to  rest  he  finds  himself  very 
much  dazed  and  confused,  though  usually  does  not  suffer 
much  pain.  He  frees  himself  or  is  extricated  from  the 
wreck,  and  may  assist  in  rescuing  others,  or  may  at  once 
go  to  some  place  of  shelter.  If  there  are  houses  near  by  he 
usually  walks  to  one  of  them,  unless  he  has  been  severely 
wounded.  If  the  accident  has  occurred  in  the  open  coun- 
try, away  from  any  habitations,  he  may  be  exposed  to  the 
weather  until  assistance  arrives.  He  is  usually  nauseated, 
and  may  vomit,  and  sleeps  badly  the  following  night.  In  a 
day  or  two  he  begins  to  have  pain  in  the  back.  From  that 
time  on  occur,  in  varying  degrees,  the  symptoms  of  neuras- 
thenia. The  history  will,  of  course,  vary  with  the  kind  of 
accident,  but  the  salient  features  of  it  are  usually  that  the 
patient  was  at  first  more  frightened  than  hurt,  and  that  the 
symptoms  only  appeared  some  time  after  the  accident. 

The  mental  symptoms  constitute  the  most  character- 
istic feature  of  the  disease.  In  the  milder  forms  the  fret- 
ful, querulous  invalid  may  be  regarded  as  hypochondriacal 
but  not  as  out  of  his  mind.  When  the  symptoms  are  de- 
veloped in  .  their  highest  degree  they  bring  the  patient 
very  near  to  the  border  land  of  insanity.     The  neurasthenic 


236  FUNCTIONAL   EFFECTS   OF   INJURY. 

is  irritable,  introspective,  depressed,  and  inattentive ;  he 
quickly  tires  of  any  prolonged  effort ;  he  is  emotional  and 
fearful,  and  does  not  sleep  well.  A  previously  strong,, 
healthy,  and  active  man  may,  after  some  trivial  accident, 
become  entirely  changed.  Little  things  which  previously 
passed  unnoticed  become  matters  of  annoyance.  Slamming 
of  doors,  loud  talking,  slight  jars  and  noises,  become  to  him 
unbearable.  An  unexpected  sound  may  cause  his  heart  to 
palpitate  very  violently.  Strong  light  hurts  his  eyes.  He 
likes  best  to  sit  or  lie  in  a  darkened  room,  removed  from  all 
causes  which  may  irritate  him.  Some  patients  take  to  their 
beds  almost  immediately  after  the  accident,  and  stay  there 
for  weeks  or  months.  In  a  case  which  I  saw  in  consultation 
with  Dr.  A.  W.  Warden,  in  reference  to  a  claim  on  the  Met- 
ropolitan Traction  Company,  the  patient  remained  in  bed 
for  many  months. 

She  was  a  single  woman,  thirty-eight  years  of  age,  of  neurotic 
temperament,  who,  previously  to  the  accident  had  always  been  rea- 
sonably well.  On  May  13,  1896,  an  open  car  in  which  she  was  sit- 
ting was  struck  by  a  cable  car.  The  jar  was  considerable  and 
the  woman  was  thrown  forcibly  against  the  back  of  the  seat. 
She  was  very  much  frightened,  but  was  not  thrown  from  the 
seat,  nor  did  she  experience  any  severe  pain  at  the  time.  She 
felt  sick  and  faint,  but  was  able  to  walk.  She  went  immediately 
to  bed,  where  she  stayed  for  five  months,  a  prey  to  the  customary 
neurasthenic  symptoms.  Pain  in  the  back,  difficulty  in  urinating 
(partly  due  to  a  pre-existing  retroversion  of  the  uterus),  difficulty 
in  breathing,  nausea,  vomiting,  and  flushings  of  the  face  were,  at 
one  time  or  another,  prominent  symptoms. 

Our  examination  in  August  failed  to  detect  any  evidences  of 
organic  nervous  injury.  There  was  no  anaesthesia,  no  limitation 
of  the  visual  field,  no  paralysis,  no  disturbances  of  the  functions 
of  the  bowels  or  bladder,  except  such  as  might  be  explained  by 
the  local  pelvic  conditions.  The  patient  was  depressed,  tremu- 
lous, and  anxious.  The  back  was  hypersensitive  m  its  whole  ex- 
tent. Pressure  on  the  vertebral  spines  in  the  thoracic  and  lower 
cervical  regions  caused  very  decided  expressions  of  pain.  The 
patient  could  walk,  but  was  afraid  to  do  so.     The  gait  was  slow^ 


TRAUMATIC   NEURASTHENIA. 


237 


hesitating,  and  uncertain.  She  complained  of  dizziness,  but  could 
stand  perfectly  well  with  closed  eyes.  The  after-history  is  in- 
teresting. From  the  time  of  the  accident  until  October — five 
months — the  patient  was  in  bed.  In  October  she  began  to  walk  a 
little  about  the  house,  and  in  November  her  claim  was  satisfac- 
torily adjusted.  But  after  receiving  the  money  the  improvement, 
instead  of  continuing,  stopped,  and  in  February,  1897,  Dr.  Warden 
told  me  that  she  was  in  bed  again,  worse  than  she  ever  had  been. 

The  neurasthenic  is  fretful,  fault-finding,  and  peevish. 
His  chief  interest  is  in  matters  directly  connected  with  his 
own  condition.  He  observes  all  his  symptoms,  and  from 
superficial  reading  of  medical  books  he  often  thinks  himself 
the  victim  of  innumerable  diseases.  While  solicitude  for 
his  family  or  his  business  is  usually  not  lost,  it  is  made  to 
yield  the  foremost  place  in  his  thoughts  to  the  anxiety  about 
his  own  health. 

Introspection  is  an  almost  constant  symptom.  The  pa- 
tient notes  and  speculates  upon  the  variations  in  his  feelings. 
He  talks  the  most  willingly  to  those  who  will  listen  the  most 
patiently  to  his  complaints.  He  constantly  visits  the  physi- 
cian, though  he  is  rarely  satisfied  with  one,  but  goes  from 
one  doctor  to  another.  Any  one  who,  even  when  in  fairly 
good  health,  is  persistently  on  the  alert  for  some  deviation 
from  the  normal  of  his  own  physiology,  will  rarely  fail  to 
detect  it.  But  the  healthy  mind  can  usually  satisfactorily 
account  for  and  dismiss  without  thought  such  trivial  symp- 
toms as  a  slight  palpitation  of  the  heart  or  an  irregularity 
of  the  digestive  apparatus.  The  neurasthenic  thinks  over 
such  symptoms,  and  through  constant  attention  they  are  apt 
to  be  made  worse.  As  a  consequence,  he  becomes  depressed. 
Neurasthenic  depression  is  different  from  the  depression  of 
melancholia,  although  these  two  conditions  may  occur  to- 
gether. In  neurasthenia  the  depression  is  in  regard  to  the 
patient's  own  prospects  and  chances  of  recovery.  Unlike 
the  melancholiac,  the  neurasthenic  rarely  loses  hope  of  ulti- 
mate restoration  to  health,  but  he  is  discouraged  at  its  long 


238  FUNCTIONAL   EFFECTS   OF   INJURY. 

postponement.  Every  new  symptom,  or  every  aggravation 
of  a  pre-existing  symptom,  adds  to  his  low  spirits.  Yet  he 
rarely  becomes  absolutely  despairing.  If  suicide  occurs,  it 
is  probably  the  result  of  something  more  than  traumatic 
neurasthenia  in  a  person  previously  well. 

Added  to  these  symptoms  are  often  many  others,  the 
most  characteristic  of  which  is  mental  fatigue.  The  neuras- 
thenic mind  usually  becomes  quickly  tired,  and  is  incapable 
of  prolonged  effort.  The  patient  may  find  it  almost  impos- 
sible to  keep  his  attention  for  any  length  of  time  on  any 
subject  not  directly  connected  with  his  own  state  of  health. 
Many  cases  are  entirely  unable  to  keep  at  work.  When  a 
neurasthenic  begins  to  read,  he  soon  lays  the  book  aside. 
If  he  plays  a  game,  his  interest  is  not  in  it  and  he  quickly 
wishes  to  stop.  Besides  the  lack  of  interest  in  any  mental 
effort,  protracted  intellectual  work  is  followed  by  an  in- 
crease of  the  various  subjective  symptoms  of  which  neuras- 
thenics so  frequently  complain. 

The  will  power  may  become  impaired  through  the  com- 
bined influences  of  fear,  lack  of  interest,  and  lack  of  atten- 
tion. The  neurasthenic  can  ordinaril}^  make  the  simplest 
decisions  only  after  much  hesitation  and  doubt.  Important 
questions  to  be  acted  upon  excite  him  very  much,  and  ne 
frequently  declares  himself  incapable  of  deciding  them. 
There  is,  however,  no  real  impairment  of  intellectual  ca- 
pacity, except  such  as  may  not  be  explained  by  hesitancy 
and  lack  of  close  attention.  The  memory  remains  good, 
though  the  patient  often  believes  the  contrary.  There  is 
little  change  in  the  quality  of  the  reasoning  powers,  when 
the  patient  can  be  brought  to  use  them. 

Fear  is  a  conspicuous  symptom.  Regis  classes  the  whole 
group  of  the  morbid  fears,  which  are  insane  fears,  under  the 
head  of  cerebral  neurasthenia.  In  traumatic  neurasthenia, 
however,  the  fears  rarely  take  systematized  forms,  except  in 
so  far  as  all  circumstances  which  relate  to  the  accident  are 


TRAUMATIC    NEURASTHENIA. 


239 


held  in  dread.  It  is  unusual  to  observe  fear  of  any  one  par- 
ticular thing,  such  as  fear  of  contamination  (mysophobia)  or 
fear  of  closed  places  (claustrophobia),  or  any  of  the  various 
systematized  forms  commonly  observed  in  certain  insanities. 
In  traumatic  neurasthenia  the  condition  is  one  of  timidity 
and  shrinking,  rather  than  of  active  fear.  The  patient  is 
afraid  to  go  out  lest  he  become  dizzy  ;  he  is  afraid  to  meet 
people  lest  they  tell  him  how  badly  he  is  looking ;  he  is 
afraid  of  anything  which  causes  his  mind  to  revert  to  the 
accident  in  which  he  was  injured.  If  he  were  injured  on  a 
railway,  he  is  very  unwilling  to  undertake  a  railway  journey. 
If  in  an  elevator,  he  prefers  the  safer  method  of  walking  up- 
stairs. 

Some  head  injuries,  however,  even  when  there  are  no 
symptoms  of  fracture  of  the  skull  or  of  cerebral  concussion, 
are  followed  by  effects  similar  in  many  ways  to  the  manifes- 
tations of  cerebral  neurasthenia  as  described  by  Regis. 

Dr.  Starr  has  kindly  communicated  to  me  the  history  of  a 
your^g  man,  twenty  years  of  age,  previously  strong,  active,  and 
healthy,  who,  during  a  football  game,  was  thrown  on  his  head. 
He  was  momentarily  stunned,  but  continued  playing.  The  team 
of  which  he  was  an  important  member  was  badly  beaten,  and  its 
defeat  was,  in  part  at  least,  explained  by  the  fact  that  the  injured 
man  made  mistakes  in  the  signals  and  so  broke  up  the  whole  sys- 
tem of  team  play.  The  young  man  himself  remembered  nothing 
■of  the  latter  part  of  the  game.  After  this  injury  he  slept  badly, 
was  nervous  and  irritable  ;  a  few  weeks  later  he  suddenly  dis- 
appeared, and  nothing  was  heard  of  him  for  four  days.  When  he 
returned  to  his  family  he  could  give  no  clear  account  of  his  ab- 
sence. He  said  that  he  had  felt  as  though  some  one  were  after 
him  and  as  though  it  were  necessary  for  him  to  get  out  of  the 
way.  He  was  seen  at  this  time  by  Dr.  Starr,  who  found  him  quiet, 
■composed,  with  the  ordinary  symptoms  of  neurasthenia.  A  short 
time  after  this  the  patient  had  an  attack  of  great  excitement,  dur- 
ing which  he  felt  himself  obliged  to  go  out  and  walk,  and  felt  like 
knocking  down  every  one  he  met  in  the  street. 

Since  the  football  game,  six  years  ago,  this  young  and  appar- 
ently strong  man   has  led  a   life  of  invalidism.     He  has  wandered 


240  FUNCTIONAL   EFFECTS    OF    INJURY. 

about  to  various  water  cures  without  fixity  of  purpose  or  power 
of  concentration.  His  conduct  has  been  erratic,  and  he  is  in  con- 
stant dread  and  fear  of  indefinite  things.  There  have  never  been 
any  periods  of  unconsciousness.  He  is  depressed,  hypochondri- 
acal, and  melancholic,  and  is  said  to  have  attempted  suicide. 

In  neurasthenia  the  speech  is  sometimes  indistinct  and 
thick,  resembling  the  speech  of  the  general  paralytic.  But, 
unlike  the  general  paralj^tic,  the  neurasthenic  can  at  once 
correct  his  speech  defects  when  his  attention  is  called  to 
them,  and  then  he  can  articulate  perfectly  well.  The 
sleep  may  remain  normal.  Ordinaril}^  however,  it  is  bro- 
ken, and  in  traumatic  neurasthenia  is  frequently  attended 
with  nightmares.  The  bad  dreams  often  relate  to  the  acci- 
dent. Neurasthenics  are  very  emotional.  Sudden  noises, 
the  sight  of  trifling  accidents,  or  even  thoughts  of  the  acci- 
dent of  which  they  themselves  have  been  the  victims,  may 
be  followed  by  evidences  of  great  excitement.  Under  such 
circumstances  the  patients  become  tremulous  and  confused, 
can  speak  only  with  difficulty,  and  are  conscious  of  prse- 
cordial  oppression  and  palpitation  of  the  heart.  They  are 
rarely  subject  to  outbursts  of  laughter,  but  tears  come 
easily. 

It  is  only  in  the  severer  forms  of  the  neurosis  that  all  of 
these  symptoms  are  present.  They  var}^  in  number  and  de- 
gree in  individual  cases.  But  usually  the  picture  of  trau- 
matic neurasthenia  is  a  picture,  as  Knapp  has  said,  "of  the 
complaining,  irritable,  nervous  invalid."  When  he  tries  to 
work  he  finds  himself  incapable  of  keeping  his  attention 
upon  what  he  has  to  do.  Efforts  to  concentrate  the  atten- 
tion are  followed  by  an  increase  of  subjective  symptoms. 
He  may  be  almost  constantly  a  prey  to  the  annoyances  of 
peculiar  subjective  sensations,  and  he  describes  his  suffer- 
ings as  more  severe  than  they  really  are.  He  becomes 
alternately  hot  and  cold  ;  he  has  flushing  of  the  face,  his 
ears  ring,   he  gets  dizzy,   his   head   aches,  and  he  becomes 


TRAUMATIC   NEURASTHENIA.  24I 

confused.  As  a  result  of  the  discomfort  from  which  he  con- 
stantly suffers,  and  from  a  fear  that  any  unusual  excitement 
may  make  it  worse,  he  prefers  staying  at  home  to  going  into 
crowded  places  or  on  the  street.  He  shuns  society,  and, 
after  his  condition  becomes  generally  known,  society,  unwill- 
incr  to  listen  to  constant  complainings,  is  glad  to  shun  him. 

&  , 

In  traumatic  hysteria  the  mental  state  has  many  characteris- 
tics similar  to  those  of  traumatic  neurasthenia,  but  there  are 
also  some  differences.  The  hysteric  is  more  silent  under 
his  sufferings,  resembling  in  this  respect  more  closely  the 
type  of  melancholia.  He  broods  more,  but  he  talks  less. 
The  hysteric  has  to  be  questioned  in  order  to  find  out  the 
nature  of  his  mental  inquietude.  The  neurasthenic  describes 
his  sensations  and  feelings  with  exaggeration,  with  an  un- 
necessary elaborateness  of  detail,^and  seeks  opportunities  to 
voice  his  complaints;  the  hysteric  talks  about  them  only 
when  he  is  interrogated. 

That  some  of  the  symptoms  of  neurasthenia  might  be 
controlled  there  is  no  doubt.  But  many  of  them  are  be- 
yond the  control  of  the  patient  and  cause  him  much  dis- 
comfort. Those  thoughts  must  indeed  be  painful  which  can 
make  a  man,  previously  strong,  healthy,  and  active,  lose  all 
inclination  and  ability  for  his  work,  and  become  more  or  less 
oblivious  to  the  interest  of  his  household. 

The  facial  expression  often  tells  the  story.  It  indicates 
not  so  much  bad  health,  as  discouragement,  anxiety,  and 
fatigue.  In  it  can  be  read  the  eternal  vv^orry  and  self-ques- 
tionings which  are  going  on  in  the  mind.  The  face  may  be 
pale,  though  very  often  if  previously  the  cheeks  were  red, 
they  do  not  lose  their  color. 

It  is  a  fact,  which  is  often  hard  to  bear  in  mind,  that  the 
complaints  and  actions  of  the  neurasthenic  depend  upon 
actual  disturbances  of  the  nutrition  of  the  ganglion  cells,  for 
which  he  is  largely  irresponsible.  He  makes  the  complaints 
because  the  ganglion  cells  are  exhausted,  and  he  keeps  the 


242  FUNCTIONAL   EFFECTS   OF   INJURY. 

ganglion  cells  from  being  repaired  because  he  so  constantly 
thinks  of  his  own  troubles. 

Thus  he  finds  himself  in  a  vicious  circle.  By  constantly 
thinking  of  his  own  ills  he  renders  his  condition  worse.  Yet 
the  same  fatigue  of  nervous  tissue  which  has  caused  the 
change  in  his  character  and  health  robs  him  of  his  independ- 
ence and  prevents  him  from  withholding  his  attention  from 
the  trivial  annoj^ances  which  are  passed  over  unheeded  by 
healthy  men.  It  is  only  by  an  appreciation  of  this  fact  that 
the  neurasthenic  can  be  treated  with  the  consideration  he 
deserves,  and  not  summarily  dismissed  as  a  person  whose 
only  disease  is  too  much  thinking  about  himself. 

Most  of  the  mental  symptoms  of  neurasthenia  are  sub- 
jective. The  physician  becomes  cognizant  of  them  chiefly 
through  the  confidences  dtf  his  client ;  and  although  an  ex- 
perienced physician  can  usually  tell  in  how  far  the  recital  is 
genuine,  he  has  no  means  of  being  positive  that  all  the  com- 
plaints to  which  he  has  to  listen  are  really  believed  in  by  the 
patient.  It  is  the  fact  of  subjectivity  of  symptoms  which  in 
negligence  cases  may  tempt  men  to  become  malingerers,  and 
which  often  gains  for  the  neurasthenic  patient  the  name  of 
cheat. 

Motor  Symptoms. — Paralysis  does  not  occur  in  traumatic 
neurasthenia,  for  gross  lesions  of  brain,  spinal  cord,  or  pe- 
ripheral nerves  are  absent,  and  functional  paralyses  occur  ex- 
clusively as  a  result  of  hysteria.  Yet,  although  no  individual 
muscle  or  group  of  muscles  completely  lose  their  powers,  or 
present  degenerative  electrical  reactions  or  atrophy,  the 
vitality  of  the  whole  muscular  system  is  very  much  lowered. 
Muscular  force  is  only  slightly  impaired.  A  more  striking 
symptom  is  the  quickness  with  which  the  muscles  become 
fatigued.  Single  movements  may  be  performed  with  nearl}''  all 
their  original  energy,  but  muscular  power  rapidly  becomes 
exhausted.  The  muscular  fatigue  can  not  be  referred  to  the 
muscles  alone.     In  every  voluntary  movement  the  stimulus 


TRAUMATIC   NEURASTHENIA. 


24S 


passes  from  brain  cortex  along  nerve  fibers  to  muscles  ;  and 
in  the  muscular  fatigue  of  neurasthenia  all  these  elements — 
nerve  cell,  nerve  fiber,  and  muscle  cell — share  ;  so  that  the 
apparent  muscular  weakness  of  neurasthenia  is  only  another 
expression  of  the  general  condition  of  the  nervous  system  in 
that  disorder.  When  the  muscles  become  tired  there  is  in- 
variably an  increase  of  other  symptoms  ;  the  general  nerv- 
ousness becomes  worse  and  the  subjective  discomforts  are 
intensified.  The  speed  with  which  the  muscles  tire  may  be 
seen  in  many  ways.  Sometimes  on  standing  only  for  a  few 
moments  the  legs  seem  to  give  way,  or  there  is  often  some 
shaking  of  the  body  when  the  eyes  are  closed.  The  gait, 
except  in  so  far  as  it  is  affected  by  lumbago,  presents  nothing 
unusual.  The  patient  moves  slowly,  but  he  lifts  his  feet 
from  the  floor  and  walks  steadily.  He  can  not,  however, 
walk  far.  A  man  who  before  the  accident  could  walk 
miles  without  fatigue,  may  become  extremely  exhausted  by 
the  walk  of  a  few  blocks.  Some  patients  walk  little  or  not 
at  all  for  many  months.  The  muscular  efforts  necessary  for 
the  performance  of  the  ordinary  duties  of  the  toilet  are  very 
fatiguing,  and  the  patient  may  be  obliged  to  sit  down  several 
times  while  dressing  himself.  The  finer  co-ordinated  move- 
ments of  the  fingers  are  imperfectly  performed.  There  is 
difficulty  in  writing,  in  buttoning  the  clothes,  etc.  This  is 
partly  due  to  tremor  and  partly  to  the  rapidity  with  which 
all  the  muscles,  but  especially  the  smaller  ones,  become  ex- 
hausted. 

Tremor  is  a  frequent  symptom.  It  resembles  very  closely 
the  tremor  seen  in  alcoholism  or  in  confirmed  tea-drinkers. 
It  is  fine,  rapid,  and  regular,  becomes  somewhat  more  pro- 
nounced on  intended  movements,  and  is  much  intensified  by 
emotional  influences  and  by  fatigue.  At  times  it  disappears 
altogether.  Its  most  frequent  situations  are  the  tongue,  the 
face,  and  the  hands.  The  tremor  observed  in  the  eyelids 
when  they  are  half  closed,  commonly  spoken  of  as  a  neuras- 


244  FUNCTIONAL   EFFECTS   OF    INJURY. 

thenic  symptom,  occurs  too  frequently  in  normal  individuals 
to  be  regarded  as  a  diagnostic  sign  of  any  great  value. 

Sensory  Symptoms. — Among  the  various  symptoms  com- 
plained of  in  traumatic  neurasthenia,  pain  in  the  back  is  the 
most  frequent  and  the  most  prominent.  It  exists  in  two 
forms :  First,  it  may  be  of  a  dull,  aching  character,  nearly 
constantly  present,  and  affect  the  whole  back,  or,  as  more 
commonly  occurs,  be  limited  to  the  neck  or  to  the  lower 
part  of  the  spine.  Its  most  frequent  seats  are  in  the  cervi- 
cal and  thoracico-lumbar  regions.  It  is  extremel}'^  indefinite 
in  character,  changing  about  from  day  to  day.  Even  at  the 
time  of  a  medical  examination  the  point  of  most  marked 
hypersensitiveness  to  touch  changes  its  location  by  several 
vertebras  within  a  few  minutes.  For  example,  at  the  first 
examination  the  tenderest  spot  may  be  found  over  the  spi- 
nous process  of  the  third  thoracic  vertebra,  and  ten  minutes 
later  the  seventh  thoracic  spine  is  found  the  most  sensitive. 
The  pain  is  aggravated  by  bodily  or  mental  fatigue  or  by 
digital  pressure  over  the  vertebral  spines,  and  is  generally 
similar  to  the  backache  frequent  in  simple  neurasthenia. 
Pain  of  this  character  is  in  large  part  an  expression  of 
fatigue,  and  exists  independently  of  injury  to  the  spinal  col- 
umn. 

Secondly,  and  more  frequentW  observed  in  traumatic 
neurasthenia,  is  pain  in  the  back  of  a  different  character, 
which  is  due  to  actual  back  sprain.  Our  knowledge  of  this 
condition,  in  regard  to  the  cases  resulting  from  railway 
accidents  at  least,  is  largely  due  to  Page.  The  affection 
has  come  to  be  known  as  traumatic  lumbago,  and  merits  a 
separate  description. 

Traumatic  Lumbago. 

Traumatic  lumbago,  since  it  depends  upon  actual  injuries 
sustained  by  the  vertebral  column,  can  not  be  classified 
among  functional  nervous  diseases.     Yet  it  is  so  frequent  an 


TRAUMATIC    LUMBAGO.  245 

accompaniment  of  neurasthenia,  and  so  rarely  fails  to  become 
complicated  by  neurasthenic  disturbances,  that  it  may  best 
find  its  description  at  this  place,  among  the  symptoms  of 
neurasthenia.  Lumbago  is  usually  the  first  symptom  to  ap- 
pear after  the  accident,  and  ordinarily  lays  the  foundation 
upon  which  the  functional  manifestations  are  superposed. 

The  confusion  which  for  so  many  years  existed  in  regard 
to  the  nature  of  the  nervous  disorders  which  most  frequently 
follow  railway  accidents  was  in  large  part  due  to  the  fact 
that  traumatic  lumbago  was  supposed  to  be  dependent  upon 
injury  to  the  spinal  cord.  Although  the  symptoms  are  often 
serious,  and  in  some  respects  similar  to  those  caused  by 
organic  injury  to  the  cord,  it  has  been  proved,  with  a  rea- 
sonable degree  of  certainty,  that  in  lumbago  the  spinal  cord 
is  not  injured  at  all.  Injury  to  the  spinal  cord  is  rarely  fol- 
lowed by  complete  recovery.  Complete  recovery  is  the 
rule  in  lumbago — a  disorder  which  is  never  fatal.  In  lum- 
bago there  is  no  anaesthesia,  no  loss  of  sphincter  power,  and 
no  paralysis  that  the  patient  can  not  overcome  unless  the 
nerves  have  been  stretched  or  torn  ;  when  the  spinal  cord  is 
injured  some  or  all  of  these  symptoms  are  present.  There 
is  also  now  little  reason  to  doubt  that  the  kinds  of  injury 
which  most  frequentl}^  cause  a  strain  of  the  muscles  and  liga- 
ments of  the  back  are  essentially  different  from  those  which 
cause  disturbance  of  the  contents  of  the  spinal  canal.  In- 
traspinal hemorrhage,  or  laceration,  or  other  damage  to  the 
spinal  cord  is  almost  exclusively  the  result  of  extreme  vio- 
lence. Yet,  since  such  conditions  have  occasionally  followed 
accidents  which  were  apparently  trivial,  it  can  not  be  posi- 
tively said  in  any  given  case  that  the  spinal  cord  has  escaped 
injury  until  examination  has  shown  that  its  functions  remain 
unimpaired. 

Traumatic  lumbago  itself  depends  upon  strain  or  lacera- 
tion of  some  of  the  numerous  structures  which  protect  the 
spinal  cord.     The  vertebras   through  which  the  spinal  cord 
17 


246  FUNCTIONAL   EFFECTS   OF   INJURY. 

passes  are  held  in  place  by  many  ligaments,  and  between 
each  bone  is  a  disk  of  cartilage.  The  bones  and  ligaments 
are  surrounded  by  numerous  muscles,  which  give  protection, 
support,  and  the  power  of  movement  to  the  spine.  The  es- 
sential characteristics  of  the  vertebral  column  are  flexibility 
and  strength.  Yet,  while  considerable  movement  is  possible 
in  the  spinal  joints,  especially  in  the  cervical  and  dorsal  re- 
gions, these  movements  are  limited  by  the  spinal  ligaments, 
and,  if  they  are  carried  too  far,  the  ligaments  will  be  strained 
or  torn. 

There  is  convincing  evidence  in  support  of  the  view  that 
traumatic  lumbago  depends  upon  more  or  less  extensive 
lesion  to  the  ligaments  or  muscles,  or  to  some  other  of  the 
structures  which  are  in  relation  with  the  vertebrse.  From 
the  anatomy  of  the  spinal  column  it  is  obvious  that  these 
injuries  may  easily  result  from  sudden  twists  or  wrenches  of 
the  spine,  such  as  are  so  frequently  received  in  railway  and 
similar  accidents,  or  as  may  occur  through  blows  or  falls  on 
the  back,  or  through  lifting  heavy  weights.  Also,  the  clinical 
type  of  the  affection  is  identical,  when  due  allowance  is 
made  for  differences  in  function,  with  those  observed  in  in- 
juries to  ligaments,  articular  surfaces,  and  muscles  situated 
elsewhere. 

The  symptoms  of  spinal  sprain  appear  soon  after  the  in- 
jury, though  it  is  several  days  before  they  reach  their  maxi- 
mum intensity.  The  chief  characteristic  of  the  condition, 
and  indeed  the  one  which  is  the  basis  for  most  of  the  others, 
is  pain  in  the  back.  The  pain  is  usually  not  spontaneous ; 
that  is,  if  the  patient  is  perfectly  motionless  he  may  be  fairly 
comfortable.  But  the  slightest  motion  in  the  affected  part 
causes  the  pain  to  become  active.  Now,  almost  every  move- 
ment of  the  body  causes  some  motion  in  the  spinal  joints. 
Most  movements  of  the  head  and  neck,  any  movements  of 
the  arms,  the  use  of  the  muscles  of  the  abdomen,  chest,  or 
back  to  effect  changes  in  position,  or  for  expulsive  acts,  the 


TRAUMATIC    LUMBAGO. 


247 


movements  of  the  legs — all  are  associated  with  more  or  less 
extensive  changes  of  position  in  the  spinal  column.  Simi- 
larly, slight  jars  or  shakes  are  transmitted  to  the  spine,  and 
by  causing  movements  such  as  pass  unnoticed  by  healthy 
persons,  quickly  induce  an  increase  of  pain  in  parts  which 
are  affected.  Consequently  there  are  very  few  moments  dur- 
ing waking  hours  when  these  patients  are  comfortable,  be- 
cause it  is  almost  impossible  for  any  one  to  remain  perfectly 
still  voluntarily.  The  pain  is  severe  and  real.  At  the  slight- 
est movement  the  patient  cries  out.  The  face  is  drawn  and 
expressive  of  past  suffering  and  of  apprehension  of  suffering 
to  come.  In  severe  sprains  of  the  back  the  whole  vertebral 
column,  from  the  skull  to  the  pelvis,  is  hypersensitive. 
More  commonly,  however,  the  pain  is  limited  to  certain  re- 
gions, such  as  the  neck  or  the  dorsal  region.  It  may  be 
limited  to  the  coccyx,  causing  the  condition  known  as  coc- 
cygodynia.  The  skin  over  the  painful  places  is  usually 
not  hypersesthetic,  although  sometimes  the  slightest  touches 
are  badly  borne.  As  Page  suggests,  it  is  probable  that  ex- 
treme hypersensitiveness  of  the  skin  is  due  to  the  fear  of 
being  hurt.  Previous  examinations  have  taught  the  patient 
that  manipulation  of  the  back  is  painful,  and  so  he  dreads  all 
contact,  and  may  cry  out  that  the  physician  has  hurt  his  back 
before  the  back  has  been  touched.  Deep  pressure,  however, 
either  of  the  back  muscles  or  of  the  vertebral  spines,  almost 
always  causes  pain  in  traumatic  lumbago,  although  it  does 
not  invariably  do  so  in  lumbago  which  is  not  of  traumatic 
origin.  The  muscles  are  tender  to  the  touch,  probably 
through  injury  to  the  muscle  fibers.  When  pressure  is  made 
on  any  of  the  vertebral  spines  which  are  in  the  painful  areas, 
pain,  often  very  severe,  is  felt  at  the  seat  of  pressure  chiefly, 
but  may  also  radiate  up  and  down  the  back.  There  can  be 
no  doubt  of  the  genuineness  of  this  symptom.  If,  before  the 
pressure  is  made,  the  finger  of  the  examiner  is  placed  upon 
the  pulse  of  the  patient,  it  may  sometimes  be  found  that  the 


248 


FUNCTIONAL  EFFECTS  OF  INJURY. 


spinal  pressure  causes  a  considerable  acceleration  of  the 
pulse  rate.  This  test — the  Mannkopff  test,  previously  de- 
scribed (see  page  219) — is  utilized  for  the  purpose  of  de- 
tecting simulation,  or  the  voluntary  exaggeration  of  spinal 

pain.  It  is  a  sign  of  con- 
siderable though  not  of 
unfailing  value,  and  is  not 
always  present  in  trau- 
matic lumbago.  If  the 
heart  beats  faster  when 
the  pressure  is  made,  it  is 
certain  that  there  is  either 
real  pain,  or  that  the  pa- 
tient is  genuinely  afraid 
that  he  is  about  to  be 
made  to  suffer ;  the  heart 
can  not  voluntarily  be 
made  to  materially  in- 
crease its  rate. 

The  muscles  of  the 
back  are  usually  in  a 
state  of  spasm,  a  condi- 
tion which  may  be  very 
marked.  In  a  recent  Van- 
derbilt  Clinic  case,  illus- 
trated in  Fig.  42,  the  back 
muscles  were  so  tense  that 
they  felt  like  boards. 

In  this  case  the  immobil- 
ity of  the  back  was  extreme. 
The  patient  had  received  a 
severe  fall  on  the  buttocks, 
soon  after  which  the  symptoms  became  very  marked.  Not  only 
was  the  whole  back  held  as  though  in  a  vise,  but  all  movements 
of  the  head,  arms,  and  legs  were  reduced  to  a  minimum.  In 
standing,  the  body  was  inclined  slightly  forward,  with  the  hands 


Fig.  42. — Characteristic  attitude  in  traumatic 
lumbago.     (Vanderbilt  Clinic. ) 


TRAUMATIC    LUMBAGO.  249 

pressed  against  the  thighs  ;  there  was  almost  no  change  of  posi- 
tion in  the  trunk  when  the  patient  sat  down  ;  and  in  walking,  the 
legs  were  dragged  forward  in  short  steps,  the  feet  being  watched 
with  as  much  care  as  the  rigid  position  of  the  head  permitted. 

The  attitude  usually  assumed  by  the  patient  with  trau- 
matic lumbago  is  due  entirely  to  the  pain.  He  puts  himself 
in  the  position  in  which  he  is  least  liable  to  receive  any  jar 
or  vibration,  and  which  permits  the  greatest  freedom  from 
movement  of  the  back.  Only  those  voluntary  acts  which 
involve  the  least  change  in  position  of  the  vertebral  joints 
are  undertaken.  The  spine  is  held  as  rigid  as  possible, 
which  results  in  very  characteristic  attitudes  and  move- 
ments. In  standing,  the  back  is  seen  to  be  held  perfectly 
stiff.  It  is  usually  bent  somewhat  forward,  and,  from  an  in- 
crease of  sensitiveness  on  one  side,  there  may  be  a  slight 
curvature.  To  look  up,  down,  or  around,  the  patient  bends 
or  turns  the  whole  body,  holding  the  neck  stiff.  Movements 
of  the  arms  are  performed  very  slowly  ;  if  the  patient  is  to 
stoop  down,  instead  of  stooping  in  the  ordinary  way,  which 
would  involve  bending  of  the  back,  he  usually  goes  down  on 
one  knee,  holding  the  back  perfectly  straight.  In  getting 
up  from  a  chair,  or  in  changing  the  position  of  the  body 
when  sitting  or  lying  down,  the  hands  and  arms  are  called 
into  service,  in  order  that  the  muscles  of  the  back  and  abdo- 
men may  do  as  little  work  as  possible.  In  getting  up  from 
the  floor  the  patient  may  "  climb  up  the  legs  with  the  hands," 
as  the  patients  with  progressive  muscular  dystrophy  do.  In 
getting  up  from  the  sitting  posture,  the  hands  are  placed  on 
the  thighs,  and  the  body  assisted  up  in  this  way. 

From  similar  reasons  there  may  be  striking  interferences 
with  gait.  The  patient  walks  with  slow,  hesitating  steps, 
lifting  his  feet  but  slightly  off  the  ground,  and  sometimes 
actually  dragging  one  or  both  feet.  The  interference  with 
gait,  through  pain  in  the  back,  often  has  the  appearance  of 
true  weakness  in  the  legs,  although  in  reality  the  legs  are  as 


250  FUNCTIONAL    EFFECTS    OF    INJURY. 

strong  as  ever,  and  appear  weak  only  because  the  patient  is 
afraid  to  move  them. 

In  some  patients  the  power  of  walking  is  altogether  lost 
for  a  time,  as  is  shown  by  the  following  case  which  was 
referred  to  me  for  examination  relative  to  a  claim  upon 
the  Delaware,  Lackawanna  and  Western  Railway  for  injuries 
received  in  a  collision  on  January  15,  1894  : 

The  patient  had  been  bruised  about  the  back  and  buttocks, 
and  for  two  weeks  was  in  bed  hardly  able  to  move  his  legs  at  all, 
because  every  movement  caused  such  severe  pain.  At  the  end  of 
five  weeks  he  could  turn  over  in  bed,  and  soon  after  began  to  get 
around  on  crutches,  which  he  was  obliged  to  use  for  nine  weeks. 
He  ultimately  made  a  complete  recovery. 

The  patient  often  attributes  the  interference  with  walk- 
ing to  spinal  disease.  Thus  a  gentleman  suffering  from 
typical  lumbago,  not  of  traumatic  origin,  because  he  had 
noticed  that  he  did  not  lift  his  feet  from  the  ground  with- 
out pain,  thought  he  was  suffering  from  locomotor  ataxia. 
Having  read  a  little  medicine,  he  came  to  me  to  have  his 
knee-jerks  tested.  In  traumatic  lumbago  unaccompanied 
by  any  injury  to  the  spinal  cord  or  nerve  roots,  the  reflexes 
remain  unchanged.  The  leg  is  often  held  stiff,  but  the 
knee-jerk  may  be  elicited,  although  re-enforcement  is  some- 
times necessary.  Disturbances  of  the  functions  of  the  blad- 
der and  rectum  are  occasionally  observed.  They  are  para- 
lytic in  appearance,  but  not  in  fact.  Through  the  pain 
caused  by  the  contraction  of  the  diaphragm  and  the  ab- 
dominal muscles,  the  patient  performs  the  expulsive  acts 
as  infrequently  as  possible.  Constipation  and  temporary 
retention  of  urine  are  the  results.  It  sometimes  happens 
that  there  may  be  a  little  dribbling  of  urine,  caused  by  an 
involuntary  overflow  of  a  too  full  bladder,  which  the  pa- 
tient is  afraid  to  empty  on  account  of  the  pain.  There  is 
never,  however,  any  true  incontinence  or  retention  of  urine 
or  incontinence  of  fasces. 


TRAUMATIC    LUMBAGO.  25  I 

Pain  caused  by  movements  may  make  it  difficult  for  the 
patient  to  go  to  sleep,  or  during  sleep  he  may  be  constantly 
aroused  by  the  pain. 

The  duration  of  traumatic  lumbago  is  variable.  Ordi- 
narily the  intensity  of  the  pain  on  movement  begins  to  de- 
crease after  three  or  four  weeks.  But  the  back  usually  re- 
mains sensitive  for  a  long  time,  and  in  many  cases  the  patient 
never  feels  that  his  back  is  as  strong  as  it  was  before  the  ac- 
cident. 

A  switchman,  who  was  struck  in  the  back  by  the  front  plat- 
form of  a  cable  car,  came  to  the  Vanderbilt  Clinic  four  months 
after  the  accident.  He  had  become  entirely  free  from  neuras- 
thenic symptoms ;  yet  the  pain  in  the  back,  although  much  better 
than  it  had  been,  was  still  very  annoying,  so  that  he  frequently 
had  sharp  twinges  on  sudden  movements,  and  could  not  stoop 
down  without  considerable  discomfort. 

The  severe  and  persistent  character  of  the  pain  ren- 
ders lumbago  a  somewhat  serious  affection.  By  interfering 
with  sleep,  exercise,  and  alimentary  processes,  and  by  caus- 
ing constant  suffering,  it  may  make  decided  inroads  on  nu- 
trition. By  impairing  the  general  health  and  by  constantly 
calling  the  patient's  attention  to  his  back,  it  materially  assists 
in  the  production  of  the  neurasthenic  picture.  The  patient 
becomes  unhappy  and  anxious,  broods  over  his  trouble, 
thinks  that  his  spinal  cord  is  injured,  and  believes  himself  in 
danger  of  becoming  paralyzed— a  fear  which  is  not  surpris- 
ing when  one  considers  how  closely  the  limitation  of  move- 
ment in  lumbago  may  imitate  paralysis. 

While  lumbago  is  a  particularly  frequent  accompaniment 
of  traumatic  neurasthenia,  its  occurrence  in  that  disorder  is 
not  constant,  nor  is  it  usually  so  severe  as  the  picture  which 
has  been  drawn  would  indicate. 

But  the  symptoms  are  always  the  same  in  kind,  though 
they  vary  greatly  in  degree.  In  its  exaggerated  form,  in 
which  the  back  is  held  absolutely  immobile  and  in  which 


2^2  FUNCTIONAL   EFFECTS   OF   INJURY. 

all  the  other  symptoms  are  equally  pronounced,  traumatic 
lumbago  is  distinctly  rare  and  only  occurs  as  a  result  of 
severe  injury  to  the  back,  such  as  may  cause  slight  dislo- 
cation in  the  spinal  joints,  or  injury  to  some  of  the  spinal 
nerves.    * 

It  is  much  more  common  for  the  clinical  picture  to  be 
limited  to  pain  and  stiffness  of  the  back,  which  do  not  seri- 
ously interfere  with  nutrition  or  cause  disturbances  which 
might  be  referred  to  interference  with  the  function  of  inter- 
nal organs. 

Headache  is  another  common  sensory  symptom  of  trau- 
matic neurasthenia.  It  may  affect  the  occipital  region,  and 
is  then  complained  of  by  the  patient  as  "  pain  at  the  base  of 
the  brain."  Or  it  may  be  in  the  forehead  and  over  the  eyes, 
similar  in  situation  and  character  to  the  pain  of  constipation. 
Besides  pain  there  may  be  various  peculiar  sensations  in  the 
head.  The  patient  feels  as  though  there  were  a  tight  band 
around  it,  or  as  though  he  were  wearing  a  heavy  cap — the 
casque  neurasthe'nique  of  Charcot.  There  are  frequently  sub- 
jective sensations  which  are  complained  of  as  noises  in 
the  head,  or  feelings  as  though  the  skull  were  about  to  fly 
apart.  The  mental  confusion  from  which  neurasthenics  so 
frequently  suffer  is  associated  with  a  feeling  of  lightness  and 
peculiar  sensations  in  the  head.  In  addition  to  these  some- 
what indefinite  pains,  people  suffering  from  neurasthenia  are 
frequently  subject  to  neuralgia.  The  pain  under  such  cir- 
cumstances is  a  true  neuralgic  pain,  which  follows  the  course 
of  the  nerve  trunks,  and  presents  the  painful  points  and  other 
symptoms  of  neuralgia  due  to  conditions  of  angemia  or  mal- 
nutrition. 

If,  at  the  time  of  the  accident,  any  parts  other  than  the 
head  or  back  were  bruised  or  injured  in  any  way,  pain  per- 
sists in  them  for  a  longer  time  than  it  would  in  persons  who 
are  not  neurasthenic.     The  neurasthenic  pays  so  constant  an 


TRAUMATIC    NEURASTHENIA. 


253 


attention  to  local  troubles  that  subjective  disturbances  which 
accompany  them  are  intensified  and  made  to  last  longer  than 
they  otherwise  would. 

Besides  local  pain,  there  is  almost  constantly  present  a 
general  feeling  of  fatigue  which  may  amount  to  pain.  The 
patient  says  he  "  feels  tired  all  over,"  a  sensation  much  ag- 
gravated by  exertion  or  excitement.  Hypersesthesia  is  also 
common.  As  has  been  said,  it  is  usually  present  in  the  pain- 
ful spots  of  the  back,  so  that  pressure  over  the  vertebral 
spines  is  ill  borne  and  may  cause  some  acceleration  of  pulse. 
The  skin  around  such  areas  may  also  be  hypersensitive,  al- 
though, as  Page  says,  this  is  probably  a  hypercesthesia  of 
education.  Other  regions  of  the  body  may  also  be  the  seats 
of  exaggerated  sensibility.  The  scalp  is  often  very  tender. 
It  is  usually  a  long  time  before  injured  parts  may  be  touched 
without  causing  expressions  from  the  patient  both  of  fear 
and  of  acute  pain.  The  muscles  of  the  whole  body,  espe- 
cially those  of  the  chest,  back,  and  legs,  are  commonly  sen- 
sitive to  the  touch  and  tender.  Hypersesthesia  becomes 
more  marked  after  any  fatiguing  influences. 

Anaesthesia  does  not  exist  in  single  traumatic  neurasthe- 
nia. It  is  frequent  in  hysteria,  and  occurs  sometimes  in  the 
serious  forms  of  nerve  disturbances,  which  will  be  described 
as  unclassified.  For  any  case  in  which  this  symptom  is 
present,  the  prognosis  is  graver  than  that  of  simple  trau- 
matic neurasthenia.  Neurasthenic  patients  often  complain 
of  feelings  of  numbness,  "  pins  and  needles  "  or  tingling,  but 
the  examination  shows  that  the  situation  of  these  sensations 
is  indefinite,  and  that  all  forms  of  cutaneous  sensibility  are 
perfectly  preserved.  There  are  also  various  other  subjective 
sensations  in  neurasthenia.  The  complaint  may  be  that 
there  is  a  feeling  of  shivering  without  being  cold,  or  as  if 
cold  water  were  running  down  the  back,  or  as  if  electricity 
were  being  applied,  or  of  numbness  in  the  legs  or  hands,  or 
other  peculiar  sensations  of  indefinite  character. 


254  FUNCTIONAL    EFFECTS    OF    INJURY. 

Special  Senses. — Ocular  Symptoms. — The  visual  disturb- 
ances of  this  neurosis  are  usually  considerable,  although 
there  are,  apart  from  possible  pre-existing  organic  defects 
or  disease,  no  morbid  changes  in  eye  structure.  The  pupils 
respond  quickly  to  light,  but  the  responses  become  pro- 
gressively less  prompt  and  complete  by  successive  stimula- 
tion. The  pupils  may  also  dilate  and  contract  under  psychic 
influences.  They  are  usually  moderately  dilated.  When 
light  is  thrown  into  the  eye,  the  iris  contracts  and  then 
dilates  again,  and  repeats  this  alternating  contraction  and 
dilatation  until  it  finally  comes  to  rest  in  contraction.  In- 
equality of  the  pupils  is  usually  regarded  as  indicative  of 
organic  disease.  Binswanger  says,  however,  that  inequality 
may  exist  in  neurasthenia  without  indicating  organic  dis- 
ease if  the  pupils  continue  to  react  promptly  to  light.  The 
complaints  of  the  patient  relate  to  various  disagreeable  sub- 
jectives  feeling  referred  to  the  eyes,  such  as  pain,  burning, 
flashes  of  light,  black  specks,  and  "  everything  getting  dark 
about  him."  The  eyes  are  generally  abnormally  sensitive  to 
bright  light,  and  they  soon  become  painful  from  use.  The 
picture  of  the  nervous  invalid,  sitting  with  the  back  to  such 
light  as  may  be  admitted  through  tightly  closed  blinds,  is 
generally  familiar. 

Asthenopia,  or  weakness  of  vision,  is  the  most  constant 
visual  disturbance  of  the  disorder.  The  eyes  quickly  be- 
come fatigued,  so  that  the  patient  no  longer  sees  perfectly. 
After  short  efforts  at  reading  or  writing  the  letters  and  words 
become  indistinct.  The  rapidity  with  which  fatigue  follows 
any  attentive  use  of  the  eyes  interferes  very  seriously  with 
vision.  The  patient  feels  as  though  there  were  a  veil  before 
the  eyes,  and  he  complains  that  they  are  blurred.  Tests 
with  the  perimeter  show  that  the  visual  disturbances  de- 
pend, in  part  at  least,  upon  fatigue  of  the  retina,  especially 
in  its  peripheral  portions.  By  successive  or  continuous  ex- 
ercise of  its  functions  the  retina  loses  some  of  its  peripheral 


TRAUMATIC    NEURASTHENIA. 


255 


power.  Thus  the  visual  field  is  smaller  the  second  time  it 
is  tested  than  it  was  the  first,  smaller  the  third  time  than  it 
was  the  second.  By  repeated  tests  the  field  may  become 
very  much  contracted,  or  the  patient  may  lose  the  power  of 
concentrating  the  attention  upon  the  testing  object.  This 
symptom  of  retinal  fatigue  has  been  called  by  Forster  the 
"  shifting  type  of  contraction  "  (Fig.  43).  The  most  conven- 
ient method  for  its  determination    has  been  described    by 


L.B. 


R.B. 


Fig.  43. — Shifting  type  of  contraction  of  the  visual  fields  in  neurasthenia.     (After  Bass.) 

Wilbrand  and  Sanger.  By  this  method  the  testing  object  is 
moved  along  the  horizontal  meridian  of  the  perimeter  from 
without  inward  to  the  center,  and  is  then  continued  across  to 
the  limit  of  the  field  on  the  nasal  side.  The  horizontal  ex- 
tent of  the  field  before  it  has  become  fatigued  is  thus  ascer- 
tained. The  object  is  then  moved  in  the  same  meridian, 
across  the  field  back  to  the  temporal  side.  If  the  retina  is 
easily  fatigued,  the  testing  object  will  on  its  return  outward 
have  ceased  to  be  perceived  before  it  has  reached  the  tem- 
poral periphery  of  the  original  field.  A  similar  limitation 
will  be  found  on  the   nasal  side  when  the  object   is  again 


256  FUNCTIONAL    EFFECTS    OF    INJURY. 

moved  inward.  The  shifting  type  of  limitation  is  the  same 
for  colors  as  for  form.  There  is  never  a  reversal  of  the  nor- 
mal color  fields,  such  as  is  found  in  hysteria. 

Limitation  of  the  visual  fields  through  fatigue  may  occur 
to  a  certain  extent  in  normal  individuals,  but  the  rapidity 
and  extent  of  the  contraction  in  neurasthenia  are  charac- 
teristic. 

In  neurasthenia  the  acuity  of  central  vision  is  not  im- 
paired. 

Of  the  other  special  senses,  taste  and  smell  are  not  af- 
fected. Organic  disease  of  the  auditory  apparatus  forms  no 
part  of  the  neurasthenic  picture.  Hypersensitiveness  of 
hearing  is,  however,  a  prominent  symptom,  which  becomes 
much  intensified  by  any  local  ear  disturbance.  The  hearing 
is  often  remarkably  acute.  A  neurasthenic  patient  of  Bin- 
swanger's  is  said  to  have  been  able,  while  sitting  in  the 
house  with  the  windows  closed,  to  distinguish  her  husband's 
footsteps  from  the  noises  of  the  street,  and  to  recognize  the 
individual  voices  of  servants  who  were  talking  two  stories 
below.  In  many  cases  of  neurasthenia  slight  noises  are 
heard  so  distinctly  that  they  become  sources  of  considerable 
annoyance,  and  may  add  to  the  severity  of  the  other  symp- 
toms. 

The  ear  is  also  frequently  complained  of  as  being  the 
seat  of  various  abnormal  subjective  sensations,  which  are  de- 
scribed as  ringing,  buzzing,  and  other  peculiar  noises.  They 
are  often  very  troublesome,  and  become  more  intensified  by 
general  fatigue  or  by  any  temporary  disturbances  of  health. 
Dizziness  is  another  symptom  which  may  be  referred  to  the 
ear.  It  is  of  nearly  constant  occurrence  in  neurasthenia,  but 
it,  too,  is  subjective  rather  than  objective.  The  patient 
complains  that  his  head  feels  dizzy,  that  objects  spin  around 
before  him,  that  he  is  in  constant  fear  of  falling,  and  that  he 
is  often  obliged  to  sit  down  or  to  catch  hold  of  surrounding 
objects  for  support.     Yet  the  objective  evidences  of  dizzi- 


TRAUMATIC    NEURASTHENIA. 


257 


ness  are  usually  wanting.  When  told  to  walk  or  stand,  the 
patient  can  usually  hold  himself  steadily.  Sometimes  when 
standing  with  the  eyes  closed  there  is  some  swaying  of  the 
body,  but  it  is  never  in  any  degree  proportionate  to  the 
amount  of  dizziness  and  unsteadiness  of  which  complaint  is 
made. 

Reflexes. — Neither  the  superficial  nor  the  deep  reflexes 
are  ever  lost  in  simple  traumatic  neurasthenia.  When  the 
reflexes  are  either  absent  or  diminished  it  should  excite  sus- 
picion of  more  serious  trouble  than  nervous  exhaustion. 
The  deep  reflexes  may  remain  normal,  but  in  by  far  the 
larger  number  of  cases  their  activity  is  increased.  This  in- 
crease affects  the  two  sides  equally.  If  the  reflex  of  one 
side  is  more  active  than  that  of  the  opposite  side,  it  is  sug- 
gestive of  organic  lesion.  The  knee-jerks  are  usually  very 
active,  so  that  a  slight  tap  on  the  patellar  tendon  induces 
a  quick,  forcible,  and  extreme  extension  of  the  leg.  Ankle 
clonus  occurs  very  rarely.  It  is  more  commonly  a  sign  of 
organic  disease,  and,  although  it  may  occur  in  slight  degree 
in  neurasthenia,  it  then  lacks  the  exaggerated  character  and 
prolonged  duration  of  the  contractions  seen  in  lesions  of 
the  pyramidal  tracts.  The  tendon  reflexes  of  the  upper 
extremity — the  extensor,  supinator,  triceps,  etc. — are  fre- 
quently absent  in  health.  In  neurasthenia  they  are  often 
present  or  hyperactive.  There  is  no  standard  by  which  the 
normal  activity  of  the  superficial  reflexes — cremaster,  epi- 
gastric, abdominal,  etc. — can  be  determined.  Some  of  them 
ma}'  be  absent  in  normal  persons.  In  neurasthenia  they  are 
usually  lively.  If  there  is  pain  or  hypersesthesia  of  one  side 
of  the  body,  there  may  be  an  increase  of  superficial  reflex 
activity  on  that  side.  The  reflexes,  both  superficial  and 
deep,  share,  with  the  other  symptoms  of  neurasthenia,  the 
common  characteristic  of  becoming  quickly  fatigued.  With 
successive  blows  on  the  tendon,  the  knee-jerk  becomes  pro- 
gressively less,  and  may  finally  cease  to  respond  altogether. 


258  FUNCTIONAL   EFFECTS   OF    INJURY. 

The  superficial  reflexes  also  quickly  tire  in  the  same  way. 
Fatigue  of  reflexes  may  be  induced  in  health,  but  in  neuras- 
thenia it  supervenes  much  more  quickly. 

Vascular  Disturbances. — Very  few  sufferers  from  trau- 
matic neurasthenia  escape  some  disturbances  of  the  circula- 
tion, of  which  the  most  common  is  palpitation  of  the  heart. 
This  neurasthenic  palpitation  is  not  due  to  disease  of  the 
heart  itself,  for  that  organ  is  normal  in  size  and  has  no  mur- 
murs. Attacks  of  palpitation  are  sometimes  sufificiently 
severe  to  resemble  the  attacks  of  angina  pectoris,  so  that  dur- 
ing them  the  whole  prsecordium  is  made  to  vibrate  by  the 
tumultuous  action  of  the  heart,  and  pulsation  in  the  super- 
ficial vessels  is  plainly  visible.  The  pulse  beats  may  be  as 
frequent  as  one  hundred  and  thirty  to  one  hundred  and  fifty 
to  the  minute,  or  it  may  even  be  impossible  to  count  them. 
The  pulse  is  quick,  soft,  and  full,  often  intermittent  and  ir- 
regular, without  any  increase  of  arterial  tension.  Pain  over 
the  heart  felt  during  the  palpitation  is  often  very  severe. 
The  patient  becomes  alarmed,  his  face  is  anxious  and  drawn, 
he  gasps  for  breath,  although  there  is  rarely  any  true  dysp- 
noea, and  he  experiences  a  variety  of  abnormal  sensations 
which  he  refers  to  the  prsecordial  region. 

These  attacks  occur  in  varying  degrees  of  severity.  It 
is  only  rarely  that  there  is  any  danger  of  confusing  them 
with  those  of  true  angina  pectoris,  a  condition  due  to  mor- 
bid changes  in  the  arteries  or  walls  of  the  heart.  In  true 
angina  pectoris  the  patients  are  usually  of  an  age  when 
arterio-sclerotic  changes  are  most  common,  some  evidences 
of  which  may  often  be  found.  In  that  condition,  also,  attacks 
come  without  apparent  cause,  and  the  pain,  which  exists  for 
some  time  before  there  appears  any  irregularity  of  the 
action  of  the  heart,  usually  radiates  from  the  left  shoulder 
down  the  left  arm.  In  neurasthenia,  pain  occurs  more  fre- 
quently after  than  before  the  palpitation,  and  for  neurasthe- 
nic palpitation  there  can  usually  be  found  some  immediate 


TRAUMATIC    NEURASTHENIA.  250 

exciting  cause,  although  it  is  often  trivial.  Sudden  noises, 
fright,  or  any  slight  mishap  often  bring  on  an  attack.  The 
mere  thought  of  the  accident  often  causes  the  heart  to  beat 
violently,  and  the  patient  may  awake  from  a  bad  dream  to 
find  that  even  in  sleep  psychic  influences  have  acted  upon 
the  innervation  of  the  heart.  In  addition  to  palpitation  the 
heart  action  in  neurasthenia  may  apparently  remain  accel- 
erated for  long  periods  of  time,  beating  ninety  or  one  hun- 
dred or  even  more  times  in  a  minute. 

In  connection  with  long-continuing  neurasthenic  tachy- 
cardia arises  the  question,  Does  it  lead  to  structural  altera- 
tion in  the  heart  muscle  ?  Oppenheim  reports  cases  which 
seem  to  have  resulted  in  this  way,  and  Knapp  inclines  to 
this  view.  That  in  neurasthenia,  even  when  the  patient  is 
at  rest  and  undisturbed,  the  heart  may  beat  a  little  more 
rapidly  than  usual,  is  possible,  although  difficult  of  proof. 
But  that  such  an  increase  in  the  pulse  rate,  unaccompanied 
by  other  factors,  ever  leads  to  hypertrophy  and  dilatation  of 
the  heart,  seems  a  matter  of  considerable  doubt.  It  may  as- 
sist in  the  development  of  a  pre-existent  tendency  to  cardiac 
degeneration,  or  it  may  accentuate  symptoms  which  had 
passed  unobserved.  But  it  is  difficult  to  believe  that  a  per- 
son whose  vascular  system  was  previously  normal  is  in  any 
danger  of  disease  of  the  heart  walls  from  neurasthenia  alone. 
Undoubtedly  cases  occur  in  which  cardiac  hypertrophy  and 
dilatation  become  apparent  while  the  patient  is  being 
treated  for  neurasthenia.  Disease  of  the  blood-vessels, 
which  existed  before  the  accident,  and  which  would  have 
eventually  become  marked  by  clinical  signs  even  if  the  pa- 
tient had  never  become  neurasthenic,  is  the  most  probable 
explanation  of  such  phenomena. 

The  other  vascular  symptoms  of  neurasthenia  may  be 
referred  to  impairment  in  the  capillary  circulation.  The 
patient  is  frequently  subject  to  sensations  of  heat  and  cold 
and  to  sudden  flushings  of  the  whole  body.    The  face  may 


26o  FUNCTIONAL   EFFECTS   OF    INJURY. 

be  observed  to  become  successively  red  and  pale.  The 
hands  and  feet  are  often  cold,  and  may  be  blue  and  feel 
numb.  Sweat  is  increased  in  amount,  and  the  patient  may 
break  out  into  perspiration  as  a  result  of  slight  excite- 
ment. 

Digestive  Disturbances. — Digestive  disturbances  are  fre- 
quent in  neurasthenia  whatever  its  origin,  and  in  many  cases 
it  seems  as  though  the  nervous  symptoms  were  in  large 
part  due  to,  or  aggravated  by,  an  auto-intoxication  from 
the  absorption  of  poisonous  substances  derived  from  im- 
perfect metabolism.  In  traumatic  neurasthenia  the  appetite 
may  be  impaired  for  some  time  after  the  accident,  although 
it  usually  soon  becomes  restored  to  the  normal  standard, 
even  when  the  nervous  symptoms  are  getting  worse.  The 
tongue  is  coated  and  tremulous  and  the  breath  is  offensive. 
The  various  symptoms  of  gastric  dyspepsia  are  frequent. 
There  are  peculiar  subjective  sensations  referred  to  the 
stomach,  such  as  feelings  of  hunger,  or  as  though  the  stom- 
ach were  constantly  empty,  or  as  though  there  were  some- 
thing gnawing  at  it.  Gastric  pain,  particularly  after  eating, 
is  the  subject  of  frequent  complaint.  Vomiting  may  occur 
immediately  after  the  accident,  but  it  rarely  continues  as  a 
symptom  later  in  the  disorder.  There  is  usually  a  consider- 
able production  of  gas  after  eating.  The  gastric  symptoms 
are  commonly  associated  with  palpitation  of  the  heart.  A 
full  meal  may  cause  the  heart  to  beat  violently  for  a  consid- 
erable length  of  time.  The  skin  may  be  sallow  and  yellow, 
but  there  is  rarely  any  jaundice.  The  bowels  are  consti- 
pated as  a  rule.  Constipation  may  have  originally  occurred 
as  a  result  of  lumbago,  but  it  also  exists  independently  of 
lumbago,  and  may  persist  after  the  pain  in  the  back  has  in 
large  part  disappeared.  In  rare  cases  occurring  after  acci- 
dents there  is  persistent  diarrhoea,  which  can  not  be  ex- 
plained by  other  than  nervous  causes.  In  the  milder  de- 
grees of  the  neurosis  the  general  nutrition  is  not  materially 


TRAUMATIC   NEURASTHENIA.  261 

interfered  with.  In  severe  cases,  however,  there  may  be 
considerable  loss  of  weight. 

The  remaining-  symptoms,  although  they  may  be  much 
complained  of,  are  of  secondary  diagnostic  importance.  In 
the  female  there  may  be  interference  with  the  menstrual 
function.  Neurasthenic  men  commonly  notice  that  their 
sexual  power  is  becoming  diminished,  and  the  desire  for 
sexual  intercourse  is  usually  lessened.  They  fear  "  loss  of 
manhood."  The  urine  shows  no  characteristic  changes.  It 
is  often  neutral  or  alkaline  in  reaction,  so  that  the  phosphates 
precipitate  readily.  The  patient,  who  observes  all  his  symp- 
toms, does  not  fail  to  ascribe  a  sinister  meaning  to  this.  He 
thinks  he  has  spermatorrhoea  or  Bright's  disease.  The  urine 
may  be  somewhat  lessened  in  quantity. 

Prognosis. — The  prognosis  of  traumatic  neurasthenia  as 
regards  life  is  very  good.  It  is  doubtful  if  a  previously 
healthy  man  ever  dies  from  the  result  of  an  accident  in 
which  he  has  received  no  injury  more  vital  than  a  sprain 
of  the  back  or  a  nervous  shock.  In  persons  whose  previous 
health  was  impaired,  or  who  were  suffering  from  actual  dis- 
ease, the  effects  of  injury  and  shock  are  much  more  serious 
and  may  sometimes  prove  fatal.  Although  many  patients 
have  died  during  the  course  of  traumatic  neurasthenia,  it 
seems  more  reasonable  to  suppose  that  in  such  cases  the  ac- 
cident added  an  impetus  to  the  progress  of  pre-existing  dis- 
ease, or  that  the  shock,  injury,  and  resulting  exhaustion 
proved  to  be  more  than  a  previously  enfeebled  organism 
could  combat. 

Persons  who  are  diseased  or  enfeebled  from  any  cause 
are  heavily  handicapped  in  the  struggle  for  life,  and  acci- 
dents or  other  injurious  influences  which  may  seem  to  fatally 
turn  the  fate  against  them  must  be  regarded  as  contributing 
rather  than  as  sole  causes.  So  the  prognosis  of  traumatic 
neurasthenia,  as  far  as  life  is  concerned,  is  generally  good, 
and  only  becomes  serious  in  the  debilitated  or  diseased. 


262  FUNCTIONAL   EFFECTS   OF   INJURY. 

It  is  very  difficult  to  arrive  at  any  satisfactory  conclusion 
regarding-  the  prognosis  for  recovery.  Different  men  hold 
different  views  relative  to  the  percentage  of  complete  recov- 
eries, and  to  the  average  duration  of  the  disorder.  The 
railway  surgeon  regards  the  prognosis  as  good  in  nearly  all 
of  the  cases.  The  neurologist,  on  the  other  hand,  takes  a 
graver  view  of  the  prospects  for  a  return  to  health.  To  see 
how  widely  opinions  on  this  subject  may  vary,  it  is  only 
necessary  to  turn  from  the  writings  of  Page  to  those  of 
Oppenheim.  Page  believes  that  most  of  the  patients  get 
well  upon  settlement  of  claim ;  from  reading  Oppenheim's 
book  one  might  be  led  to  suppose  that  recovery  was  ex- 
ceptional. This  diversity  of  opinion  may  be  explained,  in 
large  part  at  least,  by  the  kind  of  cases  seen  by  the  different 
observers. 

The  corporation  surgeon  sees  hundreds  of  cases  of  neu- 
rasthenia following  accidents  which  terminate  in  complete 
recovery,  either  spontaneously  or  after  settlement.  If  re- 
covery occur  spontaneously,  the  surgeon  thinks  the  patient 
had  little  or  nothing  the  matter  with  him ;  if  it  follows 
payment,  he  infers,  and  often  correctly,  that  the  symptoms 
had  been  largely  exaggerated.  Such  an  inference  is  by  no 
means  always  justifiable.  Neurasthenia  generally  improves 
after  mental  anxiety  and  worry  are  removed,  and  relief  from 
these  factors  is  in  many  cases  as  reasonable  an  explanation 
of  recovery  as  the  payment  of  the  claim.  Furthermore,  the 
corporation  surgeon,  while  he  often  hears  of  the  miraculous 
cures  which  the  company's  gold  not  infrequently  induces, 
loses  from  sight  the  vast  majority  of  the  patients  whom  he 
examines.  Upon  adjustment  of  the  claim  they  vanish  into 
obscurity,  and  there  is  no  means  of  discovering  whether 
they  continue  to  be  the  prey  of  nervous  symptoms  or  not. 
He  infers  that  their  troubles  are  over,  but  he  can  only  be 
sure  of  this  in  a  relatively  small  number  of  cases.  And  it 
is  this  fact  which  prevents  him  from  arriving  at  any  definite 


TRAUMATIC   NEURASTHENIA.  263 

estimate  of  the  percentage  of  cases  which  completely  re- 
cover. 

Page  endeavored  to  decide  the  question  as  to  the  pro- 
portion of  recoveries  and  the  duration  of  symptoms.  In  his 
tabulated  list  of  two  hundred  and  thirty-four  patients  who 
had  been  injured  on  the  London  and  Northwestern  Rail- 
way, the  inquiries  were  not  made,  in  the  larger  number  of 
cases,  until  two  years  had  elapsed  after  the  accident.  Some 
of  the  cases  he  saw  himself,  some  he  heard  about  from  other 
doctors,  or  from  outside  sources.  The  information  regard- 
ing many  of  these  cases  is  too  meager  to  be  conclusive.  But 
from  his  inquiries  it  appears  that  considerably  more  than 
one  half  of  the  patients  recovered  eventually,  although  re- 
covery was  often  delayed. 

Unsatisfactory  as  are  such  investigations  and  uncertain 
as  are  their  results,  they  constitute  the  only  means  we  have 
of  determining  exactly  how  serious  the  condition  is.  It  was 
originally  the  intention  of  the  writer  to  pursue  a  similar  line 
of  inquiry  regarding  the  injuries  to  the  nervous  system  which 
have  resulted  from  accidents  on  American  railways ;  but, 
after  considerable  reflection,  and  on  the  advice  from  various 
railway  officials,  the  plan  was  abandoned  as  impracticable. 
To  insure  absolute  accuracy  of  results,  it  would  be  neces- 
sary to  have  the  records  of  the  examinations  of  a  large 
number  of  patients  soon  after  the  accident,  as  well  as  thor- 
ough personal  examinations  made  after  a  considerable  in- 
terval of  time. 

Such  a  task,  were  it  undertaken  by  the  railway  companv, 
would  require  an  enormous  amount  of  labor ;  it  is  practi- 
cally impossible  for  a  private  individual.  It  constitutes, 
however,  the  one  means  of  determining  even  approximately 
the  number  of  persons  who  eventually  recover  entirely  from 
their  injuries.  Until  some  such  investigation  is  carried  out, 
our  views  of  the  prognosis  of  traumatic  neurasthenia  must 
be  based  upon  personal  observation  and  upon  the  communi- 


264  FUNCTIONAL    EFFECTS   OF    INJURY. 

cations  of  neurologists  and  surgeons  who  have  the  oppor- 
tunities of  seeing  large  numbers  of  these  cases. 

The  position  of  the  neurologist  is  at  the  other  extreme 
from  that  of  the  railway  surgeon.  The  persons  who  come 
to  him  are  either  claimants  seeking  an  expert  opinion  or 
patients  desiring  treatment.  Whichever  they  may  be,  they 
usually  present  evidences  of  serious  disturbance  of  nervous 
function.  It  is,  however,  unquestionable  that  the  serious 
condition  of  many  of  these  sufferers  is  due  to  the  influences 
by  which  they  have  been  surrounded  since  the  accident, 
rather  than  to  the  effect  of  the  accident  itself.  The  patients 
engaged  in  litigation  have  become  worse  through  anxiety, 
uncertainty,  and  frequent  examinations.  Those  who  come 
with  the  sole  object  of  getting  well  have  usually  been  sub- 
jected to  faulty  methods  of  treatment. 

This  is  especially  apparent  in  clinic  patients.  In  my 
opinion,  treatment  in  clinics  is  distinctly  prejudicial  to  neu- 
rasthenic patients,  and  I  have  no  doubt  that  the  severity  of 
the  symptoms  in  some  of  the  clinic  cases  which  have  been 
reported  to  show  how  rebellious  an  affection  traumatic  neu- 
rasthenia may  be,  even  when  unassociated  with  litigation,  was 
in  large  part  due  to  the  injurious  influences  which  every 
clinic  exerts  on  such  cases.  The  patient,  while  awaiting  his 
turn,  discusses  his  case  and  his  S3^mptoms  with  other  pa- 
tients. Through  the  constant  association  with  disease  and 
doctors,  his  attention  is  continually  riveted  on  personal 
troubles,  and  he  thus  often  becomes  an  incurable  and  offen- 
sive hypochondriac. 

These  patients  are  rarely  satisfied  with  one  phj-sician,  but 
usually  try  several,  either  simultaneously  or  consecutively. 
One  of  them  confided  to  me  that  he  had  been  at  one  time 
under  the  care  of  two  doctors,  who  gave  him  different  medi- 
cines. In  order  to  avail  himself  of  the  therapeutic  skill  of 
each,  he  mixed  the  separate  medicines  together  and  took 
one  half  of   the  amount  obtained    by  adding  together  the 


TRAUMATIC   NEURASTHENIA.  265 

doses  of  both  medicines !  The  evil  influences  of  clinic  treat- 
ment are  less  prejudicial  than  those  caused  by  waiting-  for 
claims  to  be  decided  upon,  but  they  are  longer  continued. 
A  claim  is  eventually  disposed  of,  and  the  patient's  anxiety 
is  then  in  large  part  relieved.  But  as  long  as  the  neuras- 
thenic has  strength  to  work,  or  money  enough  to  pay  car- 
fare, he  may  prolong  his  dispensary  treatment  indefinitely. 

However,  whatever  be  the  causes  of  the  condition,  the 
neurologist  sees  many  cases  of  traumatic  neurasthenia 
which  last  for  years,  and  many  which  seem  incurable.  Of 
twenty-nine  cases  of  "  traumatic  neurosis  "  observed  by  San- 
ger some  time  after  the  accident,  three  were  entirely  well, 
seven  had  only  slight  subjective  symptoms  and  could  work, 
eleven  were  only  partially  able  to  work,  and  eight  were  in 
statu  quo.  Richter  reports  three  cases  resulting  from  acci- 
dents, in  which  the  patients  were  inmates  of  the  Dalldorf 
Asylum.  All  of  them  had  originally  been  regarded  as  simu- 
lators. 

A  visit  to  any  large  neurological  clinic  will  convince  the 
most  skeptical  that  a  large  number  of  these  complaining 
hypochondriacal  invalids  believe  themselves  to  be  as  ill  as 
they  claim  to  be.  To  such  a  clinic  come  almost  daily  men 
who  give  no  evidences  of  having  any  grave  disease  of  the 
nervous  system,  yst  who  profess  themselves  as  entirely  un- 
able to  work.  In  such  cases  idleness  does  not  result  from 
any  hope  of  compensation.  Persons  who  have  actions  to 
bring  rarely  come  to  dispensaries  for  the  outdoor  poor.  On 
the  contrary,  inability  to  work  means  suffering  for  them 
and  their  families.  Yet  many  of  these  men  who,  previously 
to  the  accident,  had  been  active  wage-earners,  are  unable 
during  months  or  years  to  resume  their  regular  employ- 
ment. A  locomotive  engineer  has  been  coming  from  time 
to  time  to  the  Vanderbilt  Clinic  for  over  two  years.  From 
the  time  that  he  was  in  a  collision  he  has  been  unable  to  re- 
turn to  his  occupation.     He  is  a  robust,  intelligent  man,  and 


266  FUNCTIONAL   EFFECTS   OF   INJURY. 

was  not  conscious  of  any  injury  at  the  time  of  the  accident, 
nor  have  we  ever  had  reason  to  suspect  that  his  condition 
was  anything  more  than  traumatic  neurasthenia.  Yet  on  the 
slightest  excitement  or  fatigue  this  man  becomes  so  con- 
fused and  tremulous  that  he  has  abandoned  all  idea  of  trying 
to  work,  for  the  present  at  least,  and  has  gone  to  live  in  the 
country  for  a  year,  to  see  if  he  can  get  back  his  former 
strength  and  self-control.  Nammack  reports  the  case  of  a 
policeman  who  in  the  discharge  of  his  duty  was  very  much 
frightened  and  shaken  by  a  team  of  runaway  horses.  The 
man  was  not  physically  injured,  and  had,  of  course,  no 
thought  of  making  any  claim,  and  yet  after  two  years  his 
nervous  condition  would  not  permit  him  to  return  to  duty, 
and  he  was  eventually  pensioned  by  the  police  department. 
Similar  cases  are  of  not  infrequent  occurrence,  and  several 
examples  of  them  have  been  mentioned  in  preceding  pages. 

It  comes  especially  to  the  attention  of  the  neurologist 
that  the  seeming  exaggeration  of  traumatic  neurasthenia  is 
not  necessarily  dependent  upon  financial  considerations. 
Many  patients,  after  their  claims  have  been  adjusted  and 
paid,  or  their  actions  have  been  decided,  continue  to  present, 
with  very  little  variation,  the  same  old  train  of  famiHar  symp- 
toms. There  may  be  improvement  when  all  the  legal  for- 
malities are  at  an  end,  but  not  infrequently  the  symptoms 
continue  with  but  little  or  no  improvement. 

The  case  mentioned  on  page  236  grew  worse  instead  of 
better  after  settlement. 

However,  it  is  safe  to  say  that  of  the  total  number  of  per- 
sons who  develop  neurasthenia  as  a  result  of  accident,  the 
majority  recover  sufficiently  to  return  to  work. 

In  many,  the  restoration  to  health  is  complete,  so  that 
they  are  as  well  as  they  ever  were.  Others  find  themselves 
more  irritable  and  more  easily  tired  than  before  the  acci- 
dent. The  back  may  become  painful  on  fatigue  or  when 
suddenly  jarred  or  moved.     There  is  more  or  less  headache, 


TRAUMATIC   NEURASTHENIA.  267 

and  the  patients  do  not  sleep  as  well  as  they  formerly  did. 
Such  a  condition  of  nervousness  and  fatigue  may  continue 
for  many  years,  so  that  the  patient  never  feels  himself  "  the 
man  he  used  to  be."  However,  in  the  majority  of  persons 
previously  healthy  such  symptoms  eventually  pass  away 
entirely. 

There  are  other  cases,  and  the  number  of  these  is  con- 
siderable, in  which  the  patients,  from  the  time  of  the  in- 
jury, show  evidence  of  profound  nervous  disturbances.  All 
the  symptoms  of  neurasthenia  are  well  marked,  and,  instead 
of  getting  better  as  time  goes  on,  the  condition  remains  sta- 
tionary, or  seems  to  get  worse.  The  symptoms  of  trau- 
matic lumbago  may  pass  away,  but  the  insomnia,  the  tremor, 
the  despondency,  and  the  malnutrition  remain.  In  these 
cases  the  prognosis  for  ultimate  recovery  is  doubtful,  and 
many  of  them  are  never  able  to  resume  their  occupations. 

The  duration  of  the  disorder  is  consequently  variable.  It 
is  essentially  a  chronic  affection,  requiring  a  considerable 
length  of  time  for  repair.  The  larger  number  of  cases  which 
are  properly  treated  can  return  to  work  in  the  course  of  a 
few  weeks  or  months,  although  a  longer  time  may  be  neces- 
sary before  they  "feel  themselves  again."  It  is  uncertain 
just  how  long  the  symptoms  mayiast  before  it  can  be  said 
that  recovery  is  no  longer  probable.  It  varies  with  individ- 
ual cases  and  with  associated  circumstances.  Knapp  be- 
lieves the  chances  of  recovery  in  any  case  which  has  existed 
over  three  years  are  slight. 

Several  factors  very  materially  affect  the  prospects  of 
recover3^  Perhaps  the  most  important  of  these,  and  cer- 
tainly the  one  which  has  received  the  greatest  attention,  is 
litigation. 

The  worst  possible  thing  to  which  the  patient  with  trau- 
matic neurasthenia  can  be  exposed  are  the  mental  influences 
of  litigation. 

Litigation,    much    more    than    merely   entering    a   claim 


268  FUNCTIONAL   EFFECTS   OF    INJURY. 

with  willingness  to  adjust  it,  furnishes  the  very  influences 
from  which  a  neurasthenic  should  be  free.  The  anxiety, 
uncertainty,  and  delay  which  are  the  inevitable  conse- 
quences of  lawsuits,  prevent  the  patient  from  having  the 
physical  and  mental  rest  which  are  essential  to  recovery. 
His  mind  is  more  constantly  attracted  to  self-contemplation ; 
he  is  made  to  frequently  relate  his  symptoms,  and  is  re- 
quired to  pass  through  many  medical  examinations.  From 
the  nature  of  the  proceedings,  he  is  not  urged  to  go  back 
to  his  work,  even  if  he  is  able  to  do  so. 

It  is  hardly  fair  to  assume  that  the  increase  of  nervous 
symptoms  during  the  time  that  litigation  is  pending  is  en- 
tirely due  to  voluntary  exaggeration  by  the  patient,  or  that 
the  symptoms  improve  after  settlement  because  there  is  no 
longer  anything  to  be  gained  by  exaggeration.  As  has  al- 
ready  been  said,  it  is  universallv  characteristic  of  neuras- 
thenia that  the  symptoms  become  worse  through  disturbing 
influences  of  any  character.  This  is  observed  in  cases  in 
which  the  question  of  litigation  does  not  enter  at  all ;  and 
also,  the  various  nervous  disturbances  may  become  intensi- 
fied by  litigation,  not  simply  for  forensic  purposes,  but  be- 
cause litigation  itself  provides  the  very  factors  most  preju- 
dicial to  the  patient.  Similarly,  if  the  patient  improves 
when  the  suit  is  settled,  it  is  in  part,  at  least,  because  the 
anxiety  and  uncertainty  and  fatigue  have  been  removed,  not 
necessarily  by  reason  of  the  financial  gain. 

Treatment,  which  can  do  much  to  hasten  recovery,  can 
not  be  properly  carried  out  as  long  as  the  patient  remains  a 
plaintiff.  The  physicians  whom  the  patient  sees  are  experts 
rather  than  therapeutists;  the  important  question  is  detailed 
diagnosis  and  evaluation  of  symptoms  rather  than  cure.  As 
it  is  usually  months  or  years  before  a  case  is  settled,  the  pa- 
tient is  obliged  to  go  without  proper  treatment,  and  to  be 
surrounded  by  unfavorable  influences  for  a  long  time  and 
during  a  period  when  the  symptoms  are  most  amenable  to 


TRAUMATIC   NEURASTHENIA.  269 

cure.     Isolation  and  rest,  the  specifics  for  neurasthenia,  are 
impossible  in  negligent  cases. 

In  conclusion  it  may  be  said  that  the  prognosis  for  more 
or  less  speedy  and  permanent  recovery  in  any  case  of  neu- 
rasthenia is  good  if  the  patient  has  no  claim  to  bring  and 
can  put  himself  at  once  under  the  care  of  a  skillful  physi- 
cian, although  even  then  recovery  is  not  always  assured. 

Bibliography. 

Bass,  Das  Gesichtsfeld.     Stuttgart,  1896. 

Beard,  A  Practical  Treatise  on  Nervous  Exhaustion,  New 
York,  1880. 

Binswanger,  Die  P athologie  und  Therapie  der  JVeurasthenie,  Jena, 
1896. 

Forster,  Gesichtsfeldmessung  bei  Anaesthesiae  Retinae.  Kl. 
Monatsbl.  f.  Augenheilk.,  Beilage,  1877. 

Hodge,  C.  F.,  A  Microscopical  Study  of  the  Changes  due  to 
Functional  Activity  in  Nerve  Cells.     Journal  of  Morphology,  1S97 

Ibid.,  A  Microscopical  Study  of  the  Nerve  Cell  during  Electri- 
cal Stimulation.     Journal  of  Morphology,  1894. 

Kiiapp,  Traumatic  Neurasthenia.  Nervous  Diseases  by  Ameri- 
can Authors,  Philadelphia,  1895. 

Lugaro,  Sur  les  modifications  des  cellules  nerv.  dans  les 
divers  etats  fonctionels.     Arch.  Ital.  de  Biol.,  1895,  xxiv. 

Nammack,  Trans.  N.  Y.  Neurolog.  Soc,  1895. 

Oppenheim,  Die  traumatische  Neurosen.     2  Auf.    Berlin,  1892. 

Page,  H.  W.,  Raihvay  Injuries  in  their  Medico-legal  and  Clinical 
Aspects,  London,  1887. 

Regis,  Practical  Manual  of  Mental  Medicine,  Utica,  1894. 

Richter,  Berliner  Klinik,  August,  1895. 

Sanger,  Die  Beurtheilung  der  nervenerkrankungen  nach  Unfall. 
Stuttgart,  1896. 

Ibid,  Neurolog.  Centblatt.,  1892,  p.  121. 

Vibert,  La  Nevrose  traumatique.  Annates  d'hygiene  pub.  et  de 
me'd.  leg.,  1892,  vol.  xxviii,  p.  139. 

Wildbrand  and  Sanger,  Ueber  Sehstorungen  bei  functionellen 
Nervenleiden,  Berlin. 


CHAPTER   III. 

TRAUMATIC    HYSTERIA.* 

It  is  through  the  philosophical  and  clinical  studies  of 
Charcot  and  his  pupils  that  hysteria  has  come  to  be  re- 
garded as  a  distinct  disease,  which,  although  it  may  take 
many  forms  and  show  startling  powers  of  mimesis  of  other 
diseases,  has  its  own  identity  and  limitations.  It  is  true  of 
hysteria,  as  of  many  of  the  psychoses,  that  the  limitations 
are  often  difficult  to  determine.  The  manifestations  are 
essentially  psychical,  and,  when  not  pronounced,  it  is  not 
easy  to  decide  whether  they  are  to  be  regarded  as  symp- 
toms of  disease  or  as  mental  variations  within  the  limits  of 
health. 

Hysteria  major  and  hysteria  minor  are  the  divisions  of 
the  disorder  as  classified  by  Charcot.  Hysteria  major,  or 
la  gra7ide  hysterie,  is  the  type  characterized  by  convulsive 
attacks ;  it  is  infrequent  in  America.  Hysteria  minor  em- 
braces all  the  varieties  in  which  there  are  no  attacks.  This 
term,  consequently,  is  extremely  comprehensive,  since  it 
might  include  not  only  most  of  the  cases  of  traumatic  hys- 
teria, but  also  those  which  are  characterized  by  slight  men- 
tal instability,  in  which  there  may  never  have  been  any  of 
the  stigmata  or  accidents  of  the  disease. 

Just  how  comprehensive  the  conception  of  hysteria 
minor  should  be  it  is  impossible  to  determine.     Mental  sug- 

*  To  the  part  of  this  chapter  which  was  submitted  as  a  competitive  essay  was 
awarded  the  Joseph  Mather  Smith  prize  at  the  annual  commencement  of  the  Col- 
lege of  Physicians  and  Surgeons,  Columbia  University,  in  June,  1897. 

270 


TRAUMATIC    HYSTERIA. 


271 


gestibility  is  the  most  prominent  symptom  of  hysteria  ;  but 
if  we  are  to  class  as  hysterical  all  persons  who  display  this 
symptom,  it  will  be  found  that  a  large  part  of  the  world's 
population  is  a  victim  of  the  disease. 

Different  views  on  this  subject  are  held  by  different  men. 
Mobius  says  that  "  hysteria  is  simply  the  morbid  increase  of 
a  rudiment  which  is  present  in  all,  and  that  every  one  is  a 
little  hysterical.  If  this  were  not  so,"  he  aptly  adds,  "  it 
would  fare  ill  with  the  practice  of  medicine." 

Charcot  taught  that  hypnosis  is  possible  in  hysterical 
subjects  only,  and  yet  Bernheim  claims  that  he  can  hyp- 
notize ninety  per  cent  of  the  persons  he  sees.  If  both 
propositions  are  true,  the  conclusion  is  inevitable  that  hys- 
teria is  an  almost  universal  disease. 

For  us  it  is  sufficient  to  say  that  although  all  hysterical 
persons  are  suggestible,  all  suggestible  persons  do  not  pre- 
sent other  hysterical  stigmata,  and  that  more  symptoms 
than  mere  mental  suggestibility  are  necessary  before  we  are 
justified  in  making  the  diagnosis  of  hysteria. 

Inasmuch  as  we  are  entirely  ignorant  of  the  underlying 
anatomical  character  of  the  disorder,  any  definition  of  hys- 
teria is  necessarily  imperfect.  For  practical  purposes,  how- 
ever, it  may  be  said  that  hysteria  is  a  disease  of  unknown 
pathology,  affecting  the  whole  nervous  system.  The  symp- 
toms, which  may  be  permanent  or  transitory,  are  mental  and 
physical.  The  mental  symptoms  are  the  most  important, 
and  in  them  are  to  be  sought  the  explanations  of  the  phys- 
ical manifestations.  The  ph3^sical  symptoms  may  imitate 
very  closely  those  of  organic  nervous  disease,  but  they  do 
not  depend  on  any  structural  lesions  which  have  as  yet 
been  recognized.  They  are  involuntary  expressions  of  dis- 
ordered mental  states.  When  called  into  activit}^  by  trau- 
matic agencies,  the  affection  is  called  traumatic  hysteria. 

The  symptoms  of  hysteria  have  been  recognized  since 
the  days  of    Plato  and    Hippocrates.     For   many  centuries 


2^2  FUNCTIONAL   EFFECTS   OF    INJURY. 

they  were  supposed  to  be  dependent  upon  uterine  troubles, 
and  to  occur  exclusively  in  the  female.  Charles  Lepois, 
writing  in  1618,  abandoned  the  uterine  theory  and  admitted 
the  existence  of  the  disorder  in  men.  The  contributions  of 
Sydenham  to  the  subject  of  hysteria  showed  more  discern- 
ment than  any  which  had  preceded  them,  and  were  more 
valuable  than  many  of  those  which  were  to  follow.  Syden- 
ham studied  most  of  the  hysterical  stigmata.  He  admitted 
the  existence  of  hysteria  in  the  male,  giving  it  the  name  of 
hypochondriasis,  and  regarded  the  nervous  system  as  the 
seat  of  the  trouble.  Brodie,  in  1837,  recognized  that  func- 
tional paralysis  may  depend  upon  impairment  of  will  power. 
The  first  modern  treatise  on  the  subject  was  written  by 
Briquet,  in  1859. 

It  is  to  Charcot,  however,  that  we  owe  the  complete  pres- 
entation of  the  symptomatology  of  this  disease.  His  able 
mind,  comprehensive  learning,  and  extensive  experience  in 
all  branches  of  medicine  well  fitted  him  to  discern  the  errors 
of  previous  workers  in  this  department  of  neurology.  His 
rare  opportunities  at  the  Salpetriere  were  so  well  employed 
that  he  lived  to  see  hysteria  occupying  a  definite  and 
limited  place  in  clinical  medicine.  It  is  chiefly  through  his 
teachings  that  hysteria  has  been  shown  to  be  not  a  mixture 
of  affectation,  exaggeration,  and  deceit,  but  a  condition  in 
which  the  symptoms  are  involuntary  expressions  of  dis- 
ordered mental  states.  These  symptoms  are  not  assumed. 
The  paralyses,  ansesthesias,  and  convulsions  of  hysteria  are 
as  real  to  the  patient  as  though  they  had  visible  underlying 
causes. 

The  false  statements  of  hysterical  persons  are  not  neces- 
sarily willful  lies,  but  may  originate  honestly  from  halluci- 
nations or  from  losses  of  memory.  Many  of  the  physical 
symptoms  can  be  accounted  for  by  impairment  of  will 
power.  As  Paget  aptly  put  it,  in  referring  to  a  paralysis 
which  to-day  would  be  recognized  as  hysterical,  "  The  pa- 


TRAUMATIC    HYSTERIA. 


273 


tient  says,  '  I  can  not ' ;  it  sounds  like  '  I  will  not ' ;  it  really 
is,  '  I  can  not  will.'  " 

Brissaud  has  well  said  that  hysteria  is  "  one  and  indivisi- 
ble," and  in  employing  the  term  traumatic  hysteria  there  is 
no  intention  to  imply  that  hysteria  provoked  by  trauma  has 
any  essential  differences  from  the  disorder  when  it  is  due  to 
other  exciting-  causes.  But  as  all  diseases  vary  under  differ- 
ent causal  conditions,  so  hysteria  following  trauma  has  some 
characteristics  peculiar  to  itself.  These  special  characteris- 
tics are  not  sufficiently  distinctive  to  warrant  any  separation 
of  traumatic  hysteria  from  the  protean  affection ;  individual 
clinical  parallels  may  be  found  in  cases  of  hysteria  in  whatever 
way  they  may  have  developed.  Inasmuch,  however,  as  there 
are  usually  certain  circumstances  which  modify  the  disorder 
when  it  is  of  traumatic  origin,  the  following  description  will 
be  limited  to  those  forms  of  it  which  are  most  frequently 
observed  as  a  result  of  physical  injury  and  psychic  shock. 

Traumatism  as  a  cause  of  local  nervous  disturbance  with- 
out organic  lesion  had  been  recognized  by  Brodie,  Russell 
Reynolds,  Page,  Striimpell,  and  many  others.  But  to  Char- 
cot must  be  given  the  credit  of  having  established  beyond  a 
doubt  the  possibility  of  the  existence  of  hysteria  excited  by 
injury.  He  taught  that  the  functional  paralyses  and  anaes- 
thesias which  sometimes  follow  traumatisms  were  identical 
with  those  induced  or  made  to  disappear  by  hypnosis,  and 
he  formulated  the  theory  that  in  the  development  of  hys- 
teria the  influence  of  traumatism  is  an  influence  of  suofsres- 
tion.  The  shock  of  the  injury  acts  as  a  hypnotizing  agent, 
the  local  pain  or  discomfort  calls  the  patient's  attention  to 
the  part  injured  and  suggests  the  symptoms  of  paralysis  or 
contracture,  or  anesthesia,  or  whatever  the  sj^mptoms  may 
be.  (Traumatic  suggestion.)  There  are  some  objections  to 
this  theor)^  but  it  is  the  best  which  has  as  yet  been  offered. 

As  a  distinct  disease,  hysteria  is  unfamiliar  to  most 
American  physicians.     The  condition  is  comparativel}^  rare 


274  FUNCTIONAL   EFFECTS   OF    INJURY. 

in  this  country,  and  only  exceptionally  occurs  in  the  exag- 
gerated forms  observed  in  Europe.  As  a  result,  many  cases 
of  hypochondriasis  and  neurasthenia  are  classed  as  hys- 
terical when  they  are  not  hysterical  at  all.  Also,  it  too  fre- 
quently happens  that  hysterical  mimesis  is  confused  with 
voluntary  simulation,  and  that  true  cases  of  hysteria  are  re- 
garded simply  as  frauds.  With  the  increasing  general  inter- 
est in  neurology  and  with  the  more  conservative  use  of  the 
word  "hysterical,"  hysteria  may  some  day  become  in 
America  as  well  recognized  a  disorder  as  it  is  in  Europe. 

./Etiology — Predisposing  Causes. — Charcot  taught  that  hys- 
teria is  a  disease  which  only  shows  itself  in  persons  whose 
nervous  systems  are  diseased,  degenerate,  or  abused.  He 
classed  it  with  the  diseases  of  degeneracy,  and  regarded 
it  as  a  child  of  the  neuropathic  family.  He  believed  that 
predisposition  to  it  depends  upon  ancestral  defects  or  ac- 
quired enfeeblement  of  the  nervous  system,  and  that  with- 
out such  predisposition  the  disorder  could  not  exist.  The 
profound  disturbances  of  hysteria  which  may  follow  insignifi- 
cant exciting  causes  certainly  indicate  that  the  agent  provo- 
cateur can  only  produce  effects  in  a  nervous  system  already 
prepared  for  their  development.  Very  much  less  impor- 
tance is  attached  by  the  Germans  to  the  necessity  of  predis- 
position in  the  causation  of  hysteria,  and,  indeed,  to  prove  it 
is  not  always  easy. 

As  in  other  nervous  disorders,  we  may  in  many  cases 
discover  evidence  of  a  hereditary  disposition,  yet  it  often 
happens  that  such  proofs  are  not  obtainable.  In  America, 
so  many  of  the  poorer  classes  have  immigrated  as  children, 
and  know  little  or  nothing  about  their  families,  that  we 
are  frequently  unable  to  gather  any  reliable  information 
regarding  their  antecedents.  The  evidences  of  ancestral 
defects,  as  shown  by  stigmata  of  degeneration,  aside  from 
such  stigmata  as  may  properly  be  regarded  as  hysterical 
symptoms,  may  be  entirely  absent. 


TRAUMATIC    HYSTERIA.  27C 

Just  as  the  history  and  evidences  of  inherited  impairment 
of  the  nervous  system  may  be  wanting,  so  hysteria  may  de- 
velop in  persons  whose  personal  life  seems  to  have  been  free 
from  injurious  influences.  On  the  other  hand  it  can  some- 
times be  demonstrated  that  the  resisting  powers  of  the  nerv- 
ous system  have  become  enfeebled  through  the  effects  of 
disease  or  of  chronic  intoxications.  Among  the  diseases 
which  predispose  to  hysteria,  nephritis,  diabetes,  syphi- 
lis, the  continued  fevers,  and  many  of  the  affections  of  the 
nervous  system  are  prominent;  chronic  metallic  poisoning 
is  an  important  ^etiological  factor,  and  especially  poisoning 
from  lead  or  mercury,  the  latter  of  which  seems  to  be  asso- 
ciated with  such  particular  frequency  with  hysterical  stig- 
mata that  many  authors  believe  the  tremor  merciirialis  to  be 
largely,  if  not  entirely,  of  hysterical  origin  ;  hysteria  is  also 
very  frequently  found  in  victims  of  chronic  alcoholism. 
When  trauma  is  the  immediate  provoking  agent  of  hysteria, 
predisposition  appears  less  necessary  than  when  the  disease 
is  of  non-traumatic  origin.  Dana  and  Knapp  both  regard 
hereditary  factors  as  of  less  importance  when  the  disease 
follows  a  traumatism  than  when  it  is  due  to  other  exciting 
causes.  Of  twenty-one  cases  of  traumatic  hysteria  studied 
by  Berbez,  only  nine  had  undeniable  neurotic  antecedents. 

Exciting  Causes  {Agents  provocateurs^. — Of  the  various 
causes  by  which  hysteria  may  be  excited,  trauma  and  shock 
are  the  only  ones  which  concern  us  here.  Traumatic  hys- 
teria or  hystero-traumatism  has  only  been  recognized  in 
recent  years.  Although  it  was  previously  known  that  slight 
injuries  might  be  followed  by  functional  palsies  and  contrac- 
tures, it  was  not  until  1886  that  trauma  came  to  be  recog- 
nized as  one  of  the  most  frequent  of  the  agents  provocateurs 
of  hysteria.  It  was  again  by  Charcot  that  the  causal  rela- 
tionship was  made  clear.  He  also  showed  that  not  only  was 
traumatism  to  be  considered  as  an  astiological  factor,  but  as 
one  of  the  most  frequent  causes.     According  to  Berbez,  a 


2^6  FUNCTIONAL   EFFECTS   OF   INJURY. 

pupil  of  Charcot,  one  fifth  of  all  cases  of  hysteria  are  of  trau- 
matic origin. 

That  an  injury  without  being  severe  may  be  followed  by 
functional  paralysis,  or  contracture,  or  convulsions,  has  re- 
ceived abundant  clinical  verification. 

A  coachman  fell  from  his  cab,  and,  though  considerably  shaken 
up,  received  no  severe  injury;  five  days  later  he  developed  a 
brachial  monoplegia  of  the  side  upon  which  he  had  fallen.  A 
glass  polisher,  soon  after  a  slight  injury  to  the  wrist,  presented  a 
hysterical  contracture  of  the  hand.  A  mother,  in  a  fit  of  anger, 
struck  her  child  with  the  back  of  the  hand  ;  the  hand  which  had 
given  the  blow  soon  became  anesthetic  and  powerless.  All  of 
these  injuries  were  too  slight  and  inadequate  to  cause  organic 
changes  sufficient  to  account  for  the  startling  symptoms  which 
ensued. — (Charcot.) 

Far  more  important  than  the  severity  of  the  actual  injury 
are  the  circumstances  under  which  it  occurs,  and  the  patient's 
mental  state  at  the  time  it  is  received.  All  influences  which 
cause  excitement  and  fright  very  much  increase  the  probabil- 
ity of  hysteria  ensuing  as  a  result.  If,  immediately  before 
the  accident,  the  about-to-be  victim  has  an  opportunity  to  be 
frightened  by  what  is  going  to  happen  to  him,  the  mental 
impression  thus  received  accentuates  the  effects  of  the  phys- 
ical hurt.  To  both  of  these  factors — trauma  and  fright — 
mankind  has  ever  been  constantly  exposed,  and  in  our  me- 
chanical times  the  probabilities  of  injur}'  have  become  so 
many  times  multiplied  that  we  are  almost  constantly  ex- 
posed to  terrifying  accidents. 

Hysteria  is  frequently  the  sequel  of  distressing  railway 
and  similar  disasters,  in  which  the  victim  may  or  may  not 
have  been  injured.  It  is  essential  for  purposes  of  justice, 
as  well  as  for  correctness  of  diagnosis,  that  it  be  generally 
recognized  that  very  startling  hysterical  symptoms  can  fol- 
low accidents  which  have  caused  only  slight  physical  com- 
motion or  bruising. 

In  the  hysterical  phenomena  which  follow  local  injury 


TRAUMATIC    HYSTERIA.  2// 

the  influence  of  suggestion  is  evident.  It  is  the  part  injured 
which  becomes  the  seat  of  the  paralysis,  or  anassthesia,  or 
contracture.  A  blow  on  the  shoulder  is  followed  by  brachial 
monoplegia  of  the  same  side  ;  a  blow  on  the  hand  causes 
symptoms  in  the  hand  only  ;  if  the  injury  is  to  the  head, 
the  result  may  be  hemiplegia,  not  crossed,  but  on  the  same 
side  as  the  traumatism.  The  influence  of  suggestion  is  par- 
ticularly well  seen  in  the  cases  in  which  hysterical  symptoms 
are  superimposed  upon  organic  injury.  Charcot  records 
the  appearance  of  hysterical  contracture  of  the  forearm  and 
hand,  due  to  splints  which  had  been  applied  for  a  fracture  of 
the  radius.  Nerve  injuries  are  frequently  associated  with 
local  hysterical  manifestations.  In  the  following  case,  for 
the  privilege  of  reporting  which  I  am  indebted  to  Dr.  Starr,  a 
lesion  of  the  cauda  equina  was  complicated  by  astasia-abasia : 

A  woman,  twenty-seven  years  of  age,  was  injured  in  a  railway 
collision  on  July  4,  1894.  She  was  much  frightened,  felt  severe  pain 
in  the  back,  was  able  to  walk  for  a  few  minutes,  but  then  the  legs 
gave  way  and  she  sank  to  the  ground.  She  remained  unable  to 
walk  at  all  for  fifteen  months,  though  she  recovered  the  power  of 
moving  her  legs  in  all  directions  when  in  bed.  Immediately  after 
the  accident  there  was  retention  of  the  urine,  and  since  that  time 
the  control  of  the  bladder  has  been  imperfect.  The  catheter  was 
used  for  eight  months.  The  action  of  the  bowels  has  also  been 
irregular.  There  was  considerable  numbness  in  the  legs  and 
back,  at  first  with  imperfect  power  of  movement  and  rather  rapid 
atrophy  in  the  muscles  of  the  thighs  and  legs,  but  strength  and 
volume  have  returned  to  them. 

Examination,  October  2,  1895,  showed  areas  of  anesthesia 
(Fig.  44)  around  the  umbilicus  and  around  the  anus.  Though 
the  patient  had  perfect  command  of  the  legs,  and  could  move 
them  in  every  direction  while  lying  down,  astasia  was  complete, 
and  the  legs  collapsing  immediately  when  any  attempt  was  made 
to  stand.  There  were  general  neurotic  symptoms  as  well.  This 
condition  persisted  for  a  long  time  after  the  accident,  in  spite  of 
substantial  damages.  In  this  case  it  seems  that  the  astasia  was 
purely  hysterical,  while  the  anaesthesia  of  the  perineum  and  the 
bladder  and  rectal  symptoms  were  evidences  of  hcemorrhage  or 
some  organic  injury  to  the  cauda  equina. 
19 


278  FUNCTIONAL   EFFECTS   OF    INJURY. 

One  year  later  the  patient  was  seen  again,  having  in  the  mean- 
time been  taught  to  walk  with  a  roller  machine.  She  then  walked, 
perfectly,  had  no  general  hysterical  symptoms,  but  the  area  of 
anaesthesia  remained  exactly  the  same  as  before. 

When  psychic  shock  alone  is  the  exciting  cause,  the 
symptoms  are  usually  less  localized.  Under  such  condi- 
tions   the    hysterical    manifestations    are    more   commonly 


Fig.  44. — Anaesthesia  in  a  case  of  injury  to  the  Cauda  equina,  associated 
with  astasia-abasia. 


aphonia,  or  convulsions,  or  coma.  Among  the  other  factors 
having  certain  bearings  on  the  setiology  of  traumatic  h^^s- 
teria  are  sex,  age,  occupation,  race,  and  sometimes  litigation. 
Sex. — Non-traumatic  hysteria  is  much  more  frequent  in 
women  than  in  men.  The  failure  to  recognize  that  hysteria, 
may  occur  in  man  was  for  a  long  time  an  important  obstacle 
in  the  progress  of  knowledge  regarding  the  disease  ;  but  in 
the  past  few  years  its  frequent  occurrence  in  the  male  has. 
become  amply  demonstrated.  This  advance  was  largely  due 
to  the  observation  of  hysterical  stigmata  which  occurred  in 
men  as  the  results  of  accidents  and  injury.    Although  women 


TRAUMATIC    HYSTERIA. 


279 


furnish  by  far  the  larger  number  of  examples  of  non-trau- 
matic hysteria,  when  the  disorder  first  appears  as  a  result 
of  trauma,  it  seems  as  though  men  were  more  frequently 
affected  than  women.  Berbez,  in  twenty-one  cases  of  trau- 
matic hysteria,  found  that  fourteen,  or  two  thirds  of  them, 
\vere  men.  In  Knapp's  cases  the  relative  number  of  men 
and  women  was  about  equal  ftwenty-five  cases — thirteen 
women'j.  Greater  exposure  to  traumatic  influences,  acting 
as  a  predisposing  cause,  may  account  for  the  greater  fre- 
quency with  which  traumatic  hysteria  appears  in  men  than 
in  women.  However,  the  increased  proportion  of  men  to 
women  is  not  nearly  so  large  in  this  disease  as  it  is  in  trau- 
matic neurasthenia. 

Age  exerts  the  same  influence  upon  the  development  01 
traumatic  hysteria  as  upon  that  of  traumatic  neurasthenia  ; 
both  are  essentially  disorders  of  the  active  periods  of  life, 
although  traumatic  hysteria  may  occur  at  any  age,  and 
sometimes  is  present  in  children.  Profession  and  mode  of 
life,  except  in  so  far  as  they  predispose  to  impairment  of 
health,  seem  to  exercise  less  influence  than  race.  The  Ameri- 
can, who  is  so  subject  to  nervous  exhaustion,  less  commonly 
develops  hysteria  after  accidents.  In  Europe,  and  especially 
in  France,  traumatic  hysteria  is  not  uncommon.  All  over 
the  world,  Hebrews  are  a  prey  to  various  neuroses,  and  hys- 
teria is  a  common  disease  in  male  Jews.  In  fact,  the  largest 
number  of  the  cases  of  traumatic  hysteria  which  occur  in 
this  country  are  found  in  Hebrews  or  in  the  foreign-born. 

The  effects  of  litigation  have  a  somewhat  different  bear- 
ing upon  the  course  of  hysteria  than  upon  that  of  neurasthe- 
nia. In  neurasthenia  the  uncertainty  and  anxiety  of  suit 
may  make  a  serious  affection  of  what  would  otherwise  be 
trivial.  In  hysteria  the  symptoms  are  developed  soon  after 
the  accident,  independently  of  any  question  of  damages  and 
often  before  there  is  an  opportunity  for  such  a  question  to 
arise.     Neurasthenia  would  in  many  cases  not  appear  at  all 


28o  FUNCTIONAL   EFFECTS   OF    INJURY. 

if  the  patient  could  at  once  be  surrounded  by  proper  influ- 
ences only;  but  most  commonly,  when  any  one  who  de- 
velops hysteria  has  once  received  the  fright  or  the  injury, 
the  mischief  is  already  done,  and  the  disease  appears  in  its 
full  development.  The  subsequent  course  of  the  case  will 
depend  in  large  part  upon  environment,  and  will  be  pro- 
tracted or  made  more  severe  by  the  evil  effects  of  litigation. 
But  there  are  few  cases  of  traumatic  hysteria  of  which  it 
can  be  truthfully  said  that  the  symptoms  would  not  have 
appeared  except  for  the  question  of  damages. 

Pathology. — Into  theoretical  speculation  upon  the  pa- 
thology of  hysteria  it  would  be  useless  to  enter  here. 
Nothing  is  known  as  to  what  morbid  anatomical  changes 
are  responsible  for  the  symptoms  of  this  disease,  and,  fur- 
thermore, it  is  improbable  that  the  problem  will  be  solved 
by  any  of  the  microscopical  methods  at  present  at  our  dis- 
posal. As  far  as  is  known,  the  central  nervous  system  in 
hysteria  is  anatomically  normal.  That  some  morphological 
or  chemical  changes  underlie  the  alteration  in  function  there 
is  little  reason  to  doubt ;  but  the  pathology  of  hysteria  will 
prove  even  more  elusive  than  that  of  neurasthenia.  Hys- 
teria is  a  disorder  chiefly  affecting  the  mind,  and  its  location 
is  probably  cerebral ;  but  whether  it  is  entirely  cortical  or 
situated  as  well  in  other  regions  of  the  brain,  it  is  impossible 
to  say. 

Symptoms.— The  symptoms  of  hysteria  are  divided  into 
permanent  symptoms,  or  stigmata,  and  accidental,  paroxys- 
mal, or  intervallary  symptoms.  Usually  some  of  the  stig- 
mata are  constantly  present  during  the  disease ;  they  in- 
clude the  mental  state,  anaesthesia,  and  the  affections  of  the 
special  senses.  The  paroxysmal  symptoms,  as  the  name  in- 
dicates, are  only  of  occasional  occurrence,  and  embrace  the 
paralvses,  the  contractures,  the  convulsions,  and  similar 
manifestations. 

As  Briquet  very  truly  says,  "  hysteria  attacks  the  whole 


TRAUMATIC    HYSTERIA.  28 1 

organism."  Its  symptoms  may  be  those  of  disturbance  of 
function  of  any  organ.  Some  are  very  much  more  fre- 
quently encountered  than  others,  and  certain  symptoms  are 
usually  associated.  Anaesthesia  and  contraction  of  the  vis- 
ual fields  are  particularly  constant,  and  are  generally  com- 
bined. Paralysis  is  more  infrequent,  yet  when  it  occurs  it 
is  almost  invariably  accompanied  with  loss  of  sensation. 
Tremor  is  common,  especially  in  traumatic  hysteria.  Occa- 
sionally only  one  hysterical  symptom  is  present,  and  it  is  in 
such  cases  that  the  diagnosis  is  difihcult  and  uncertain,  and 
can  only  be  made  by  the  exclusion  of  other  conditions.  It 
is  in  mono-symptomatic  cases  of  traumatic  hysteria  that 
the  exclusion  of  simulation  becomes  sometimes  impossible. 
Fortunately,  for  diagnostic  ends  at  least,  traimiatic  hysteria 
is  most  frequently  revealed  by  several  characteristic  evi- 
dences, and  often  the  picture  is  so  clearly  defined  that  there 
can  be  no  doubt  as  to  its  meaning.  In  a  case  which  has  been 
under  my  care  for  some  time,  the  patient  tells  a  characteris- 
tic story  of  hysteria  which  may  or  may  not  be  true  ;  but  the 
symptoms  he  presents  are  unmistakable,  and  have  been 
abundantly  verified  by  repeated  observations.  They  are  in 
so  many  respects  illustrative  of  traumatic  hysteria  that  an 
account  of  the  case  may  be  properly  given  here : 

P.  D.,  forty-seven  years  of  age;  alcoholic,  as  was  also  his 
father;  denies  all  symptoms  of  nervous  disease,  except  alcohol- 
ism, in  all  the  members  of  his  family.  Says  he  is  an  actor  by  pro- 
fession. 

On  the  19th  of  October,  1894,  while  in  the  flies  of  a  theater,  he 
fell  twenty-eight  feet,  "landing  on  the  head  and  spine."  He  was 
in  the  hospital  for  seven  weeks,  during  the  first  half  of  which  pe- 
riod he  was  unconscious.  When  he  came  to  himself  he  found  that 
he  could  not  move  the  left  side  at  all,  and  that  the  movements  of 
the  right  hand  were  very  much  impaired.  There  was  no  loss  of 
control  of  the  bladder  or  rectum.  For  many  months  after  the 
accident  he  was  completely  aphonic ;  he  soon  recovered  consid- 
erable power  in  the  left  hand,  less  in  the  left  leg.  He  was  too 
much  disabled  to  work,  and  having  no  money,  he  was  sent  to  the 


282 


FUNCTIONAL   EFFECTS   OF   INJURY. 


Almshouse  Hospital.  The  patient  remained  in  the  Almshouse 
three  months  and  a  half,  and  during  that  time,  the  house  physi- 
cian says,  he  did  not  utter  a  sound  of  any  kind,  and  invariably 

dragged  the  left  leg 
in  walking.  He  had 
no  motives  for  simu- 
lation, and  I  believe 
that  the  patient  was 
honest  in  regard  to 
his  symptoms.  Even- 
tually leaving  the 
hospital,  this  man 
was  again  seen  in  a 
few  months  at  the 
Workhouse,  where 
he  had  been  sent  for 
drunkenness.  The 
left  leg  was  still 
dragged,  but  the  pa- 
tient had  recovered 
the  faculty  of  speech. 
He  told  us  that  he 
had  recovered  his 
voice  as  the  result 
of  falling  off  the  rear 
platform  of  a  rail- 
way car.  He  had 
been  considerably 
stunned  by  the  acci- 
dent, but  on  regain- 
ing consciousness,  he 
says,  he  "  was  scared 
to  death  by  finding 
that  he  was  talking 
to  himself."  The 
aphonia,  at  least, 
had  been  cured  !  The 
general  condition  at  this  time  (October,  1896 — two  years  after 
the  original  accident)  appears,  from  my  notes,  to  be  as  follows : 
A  well-developed  man,  slightly  anaemic.  Heart,  lungs,  and  other 
vegetative  organs  apparently  sound.  There  is  some  weakness  of 
the  left  hand,  shown  on  attempts  at  movement.     The  movements 


Fig.   45. — Traumatic   hysteria,    showing    characteristic 
dragging  of  the  foot.     (Workhouse  Hospital.) 


TRAUMATIC   HYSTERIA. 


283 


at  the  left  knee  and  ankle  joints  are  limited  by  reason  of  muscu- 
lar weakness,  so  that  the  patient  can  flex  and  extend  both  the 
foot  and  the  leg  to  a  slight  degree  only.  In  walking  (Fig.  45), 
the  left  leg  is  dragged,  as  though  it  were  an  inert  mass.  The 
toe  and  inner  side  of  the  foot  scrape  along  the  floor,  and  the 
heel  touches  the  floor  only  when  the  patient  is  standing  still. 
There  is  a  contracture  of  the  wrist  and  of  the  fingers  of  the  right 


Fig.  46.— Traumatic  hysteria.  Paralysis  existed  in  the  left  leg.  In  the  shaded  areas, 
cutaneous  sensibility  was  diminished  ;  in  the  left  leg  it  was  totally  abohshed. 
(Workhouse  Hospital.) 


hand.  The  fingers  are  held  in  extension  and  the  wrist  is  slightly 
flexed.  This  contracture  may  be  overcome,  but  attempts  at  for- 
cible movement  in  these  joints  cause  considerable  pain.  There 
are  nowhere  any  wasting  of  muscles  or  changes  to  the  normal 
reactions  of  electricity. 

From  a  point  a  very  few  inches  above  the  knee,  downward,  the 
left  leg  is  totally  ansesthetic.  The  skin  does  not  bleed  to  ordi- 
nary pin  pricks  in  the  antesthetic  area.  There  is  a  diminution  in 
the  acuity  of  cutaneous  sensibility  over  the  remaining  portion  of 
the  left  side  of  the  body  (Fig.  46).  There  is  slight  deafness  in  the 
left  ear.  The  patient  insists  that  he  sees  perfectly  well,  but  the 
visual  fields  as  marked  out  by  the  perimeter  (Fig.  47)  show  a 
moderate  contraction,  which  follows  the  periphery  of  the  normal 


284 


FUNCTIONAL   EFFECTS   OF   INJURY. 


field.  It  is  more  marked  for  the  left  eye.  The  color  fields  are 
diminished  in  extent,  but  there  is  no  reversal  of  their  normal  ar- 
rangement. 

The  patient  complains  of  no  pain  or  hypergesthesia,  with  the 
exception  of  the  pain  caused  by  movements  of  the  right  wrist. 
He  sleeps  fairly  well.  He  is  a  tractable  prisoner,  and  because  he 
walks  better  at  times  than  at  others,  he  is  generally  looked  upon 
as  a  "  fakir  "  by  the  guards. 

The  mental  condition  presents  nothing  particularly  character- 
istic.    There  have  never  been  any  emotional  manifestations,  and 


Fig.  47. — Field  of  vision  in  a  case  of  traumatic  hysteria.  The  contraction  is  more 
marked  on  the  left,  which  was  the  side  of  paralysis  and  anasthesia.  (Workhouse 
Hospital. ) 

although  at  times  the  patient  appears  discouraged  and  depressed,, 
the  neurasthenic  mental  state,  often  present  in  traumatic  hysteria, 
is  not  pronounced  in  this  case.  The  symptoms  did  not  disappear 
when  the  patient  was  intoxicated.  He  once  came  to  my  office 
very  drunk,  but  was  dragging  his  foot  in  the  same  old  way.  The 
long  period  during  which  he  has  maintained  the  same  chain  of 
symptoms,  the  absolute  lack  of  motive  for  deception,  and  the  ab- 
sence of  all  evidences  of  organic  disease,  render  the  diagnosis  of 
traumatic  hysteria  incontestable. 

There  was  a  predisposition  caused  by  alcoholism,  both  parental 
and  personal — a  consideration  which  should  have  been  taken  into- 
account  had  the  case  been  the  subject  of  medico-legal  inquiry. 


TRAUMATIC    HYSTERIA. 


285 


Mental  Symptoms. — The  most  prominent  feature  of  the 
mental  state  of  hysteria  is  the  causation  of  physical  symp- 
toms which  imitate  conditions  such  as  may  be  the  results  of 
organic  disease.  The  imitation  is  sometimes  so  close  that  it 
is  with  difficulty  that  the  true  nature  of  the  physical  dis- 
turbances may  be  appreciated.  The  mimetic  powers  of  this 
affection  are  far  more  highl}'  perfected  than  any  to  which 
the  voluntary  simulator  may  hope  to  attain,  and  differ  from 
attempts  at  fraudulent  and  voluntary  simulation  in  that  they 
are,  in  large  part  at  least,  unconsciously  performed.  In  a 
disorder  which  of  itself  is  histrionic  and  exaggerative  the 
opportunities  for  voluntary  exaggeration  and  deceit  are  con- 
siderable, and  hysterical  symptoms  become  regularly  worse 
when  they  are  observed  by  others.  The  patients,  who  are 
never  so  happy  as  when  forming  centers  of  attraction,  have 
a  tendency  to  embellish  such  of  their  clinical  manifestations 
as  are  deemed  worthy  of  special  investigation  by  learned 
men,  or  as  are  received  with  interest  by  audiences  composed 
of  physicians  and  medical  students.  It  seems  probable  that 
some  at  least  of  the  astonishing  hysterical  phenomena  which 
are  reported  from  certain  psychiatrical  clinics,  if  they  are  to 
be  considered  as  genuine  products  of  mental  disease,  'could 
only  occur  under  conditions  which  are  most  favorable  to  the 
full  development  of  the  psychosis.  Yet,  after  due  allowance 
has  been  made  for  errors  of  interpretation,  the  fact  remains 
that  psychical  mimesis  is  frequently  found  in  persons  who 
are  ignorant  of  the  existence  of  any  such  thing  as  hysteria, 
and  who,  uneducated  and  without  motive,  closely  imitate  dis- 
eases of  which  they  have  never  heard.  That  hysteria  is  dif- 
ferent from  simulation  is  proved  by  the  occurrence  of  hys- 
terical phenomena  among  all  peoples  and  in  all  times,  by  the 
general  uniformity  in  the  character  of  the  symptoms  and  by 
the  lack  of  motive  or  ability  of  simulation  in  the  majority  of 
its  victims.  Although  the  disease  is  essentially  simulative 
and  its  manifestations  unreal,  it  occurs  not  only  without  in- 


2S6  FUNCTIONAL    EFFECTS    OF    INJURY. 

tention,  but  without  the  patient  knowing  that  his  symptoms 
are  false.  It  can  best  be  explained  by  the  theory  that  it  is  a 
morbid  mental  state  which  involuntarily  and  unconsciously 
provokes  a  mimicry  of  the  symptoms  of  other  diseases.  It 
is  only  when  the  fact  is  appreciated  that  hysteria  is  a  serious 
disorder  affecting  the  mind  that  the  sufferer  from  it  can  be 
treated  with  the  consideration  he  deserves  ;  even  then  it  is 
oftentimes  difficult  to  believe  in  the  sincerity  of  a  patient 
who  is  seen  to  move  a  limb  which  was  apparentl}^  para- 
lyzed, or  who,  though  nearly  blind  to  usual  tests,  never  pays 
the  accidental  penalties  of  organic  blindness.  It  can  be 
proved  by  optical  tests  that  in  hysterical  amaurosis  sight  is 
in  reality  not  lost ;  in  the  hypnotic  state  the  patients  may 
■describe  sensations  which,  while  awake,  passed  apparently 
unperceived,  or  may  be  made  to  move  muscles  which  were 
paralyzed  ;  similarly,  by  hj^pnosis,  memory  loss  may  be 
shown  to  be  not  genuine. 

When  it  is  thus  demonstrated  that  functional  activity, 
though  apparently  abolished,  exists,  we  can  not  suppose  that 
there  are  lesions  in  the  organs  or  in  the  nerve  tracts  or  in 
the  perceiving  centers  themselves.  Janet,  who  has  studied 
this  subject  with  rare  skill,  explains  the  apparent  contradic- 
tion of  hysterical  phenomena  by  the  theory  of  a  limitation 
of  the  field  of  consciousness.  Mental  actions  go  on,  but  are 
independent  of  the  patient's  personal  knowledge.  Centripe- 
tal stimuli  may  be  perceived  by  the  perceiving  centers,  but 
they  are  not  transferred  to  the  domain  of  personal  con- 
sciousness. Centrifugal  impulses  may  be  voluntarily  liber- 
ated, but  such  volitional  impulses  originate  independently 
of  the  higher  Ego.  By  thus  assuming  a  power  of  subcon- 
sciousness, of  which  the  higher  consciousness  in  normal 
minds  is  only  occasionally  aware,  and  to  which,  in  hysteria, 
the  higher  consciousness  may  become  completely  oblivious, 
most  hysterical  symptoms  can  be  explained. 

In    non-traumatic    hysteria    the    mental    symptoms    are 


TRAUMATIC    HYSTERIA. 


287 


somewhat  different  as  they  occur  in  men  and  in  women. 
Traumatic  hysteria,  whether  occurring  in  men  or  in  women, 
has  the  characteristics  of  male  hysteria,  in  which  the  purity 
of  the  hysterical  picture  is  blurred  by  the  admixture  of 
symptoms  of  neurasthenic  conditions,  so  that  it  is  often  a 
composite  of  hysteria  and  neurasthenia,  a  circumstance 
which  has  gained  for  it  the  name  of  hystero-neurasthenia. 
In  traumatic  cases  neurasthenic  disturbances  are  particularly 
prominent  during  the  interval  between  the  occurrence  of 
the  accident  and  the  appearance  of  typical  hysterical  mani- 
festations.    A  case  of  Charcot's  well  illustrates  this : 

A  man,  fifty-three  years  of  age,  industrious  laborer,  witnesses 
the  suicide  of  his  son.  He  loses  consciousness  for  several  mo- 
ments. From  that  time  the  father  is  a  changed  man.  From  being 
gay  and  active  he  becomes  sad  and  bad-tempered.  He  shuns  the 
people  with  whom  he  used  to  be  on  good  terms.  His  sleep  becomes 
restless  and  filled  with  annoying  and  painful  dreams.  He  thinks 
•of  his  son  as  a  happy  child,  and  then  sees  him  bloody  and  dis- 
figured. The  memory  for  recent  events  fails.  The  man  becomes 
distracted.  His  head  feels  as  though  he  wore  a  heavy  cap.  The 
sexual  functions  are  weakened.  There  are  digestive  disturbances 
after  eating.  He  becomes  weak  and  easily  fatigued.  These 
symptoms  are  largely  neurasthenic  in  character,  and  they  con- 
tinue to  be  prominent  even  after  the  addition  of  paroxysmal  hys- 
terical accidents. 

Suggestibility  is  the  underlying  characteristic  of  the 
hysterical  mental  state,  whether  the  disorder  is  induced  by 
traumatism  or  by  other  causes.  The  patient  is  constantly 
subjected  to  influences  similar  to  those  used  in  induced  sleep, 
■  By  Charcot's  theory,  as  we  have  seen,  the  accident  itself 
exerts  its  influence  by  means  of  suggestion.  Hypnotism  is 
the  effect  of  suggestion  upon  a  hysterical  mind,  or  at  least 
upon  a  mind  which  is  morbidly  suggestible,  a  condition 
closely  allied  to  hysteria,  if  not  in  itself  hysterical,  and  the 
mental  symptoms  of  hysteria  and  the  manifestations  of  pro- 
voked hypnosis  are  closely  related,  if  not  identical.     B3'  this 


288  FUNCTIONAL   EFFECTS   OF   INJURY. 

theory  may  best  be  explained  the  genesis  of  the  disorder; 
by  it  also  may  be  best  understood  those  symptoms  which  are 
purely  psychical  and  the  rapid  alternations  in  the  manifesta- 
tions which  are  physical.  The  different  effects  of  auto-sug- 
gestion under  different  conditions  are  well  illustrated  by  the 
case  to  which  reference  has  already  been  made  (page  281): 
the  actor  who  fell  from  the  flies  of  a  theater  was  apparently 
but  little  hurt,  but  became,  a  few  days  later,  completely 
aphonic.  For  several  months  he  could  not  utter  a  sound, 
although  he  was  perfectly  well  in  other  ways,  aside  from  the 
hysterical  symptoms.  When  he  fell  from  the  rear  platform 
of  a  moving  railway  train  he  again  escaped  with  trifling  in- 
juries ;  but  the  impression  which  this  accident  made  upon  him 
acted  in  a  different  way  from  that  of  the  first,  for  he  imme- 
diately began  to  talk,  and  has  had  no  difficulty  in  talking  ever 
since.  In  a  person  once  hypnotized,  the  most  trifling  occur- 
rences may  act  as  suggesting  agents,  and  in  hysteria  it  some- 
times seems  as  though  these  agents  originated  in  the  patient's 
own  mind,  independently  of  external  influences.  (Auto-sug- 
gestion.) Of  similar  import  are  dreams  and  nightmares 
which  are  frequent  symptoms  of  hysteria.  When  the  disor- 
der arises  from  traumatic  causes  the  details  of  the  accident 
may  in  this  way  be  kept  constantly  in  view.  In  the  daytime 
the  patient  reflects  upon  what  he  dreamed  at  night,  thus  con- 
tinuing the  auto-suggestion.  Many  of  the  apparently  false 
statements  of  hysterical  subjects  arise  from  dreams  which 
the  patients  fail  to  differentiate  from  actual  occurrences. 

From  dreams  at  night  and  from  reveries  through  the  day 
may  arise  hallucinations.  Hysterical  hallucinations  have 
attained  medico-legal  importance  in  various  criminal  inqui- 
ries in  Europe.  They  are  not  frequent  in  traumatic  hys- 
teria ;  when  they  occur,  they  usually,  but  not  always,  relate 
to  the  accident. 

Hun  reports  a  case  in  which  they  were  an  important 
feature  : 


TRAUMATIC    HYSTERIA. 


289 


A  dressmaker,  who  was  sitting  in  the  last  car  of  a  railway- 
train  which  was  standing  before  the  station,  saw  another  train  on 
the  same  track  rapidly  approaching  from  behind.  She  was  very 
much  frightened,  and  in  trying  to  get  out  she  was  thrown  down 
and  hurt  her  back,  although  she  escaped  any  grave  injury.  She 
was  temporarily  unconscious,  but  soon  came  to  herself.  In  addi- 
tion to  the  ordinary  hysterical  symptoms  of  sensorial  angesthesia 
and  paralysis  which  resulted  from  the  accident,  this  patient  began 
to  have  recurring  attacks  in  which  she  shouted  and  "  raved  that 
she  was  in  a  lunatic  asylum,  and  begged  not  to  be  sent  upstairs  to 
the  noisy  ones."  She  also  saw  knives  and  blood  on  the  walls  of  her 
room.  The  patient  was  paid  eight  thousand  five  hundred  dollars 
by  the  railway  company,  without  litigation,  but  after  this  the 
gradual  improvement  which  had  begun  did  not  seem  accelerated. 
She  continued  to  have  from  three  to  six  attacks  of  convulsions 
each  month,  and  the  right  leg  remained  insensible  and  paralyzed. 
After  hospital  treatment  she  was  cured  of  all  her  symptoms. 

Loss  of  memory  often  gains  for  the  hysteric  the  reputa- 
tion of  a  liar  and  swindler,  and  renders  the  history  he  tells 
the  physician  unreliable  by  reason  of  faulty  and  contradic- 
tory statements.  Hysterical  amnesia  usually  differs  from 
organic  amnesia  in  its  periodicity  and  in  its  Hmitation  to 
certain  classes  of  ideas.  Janet  classifies  it  as  systematized, 
localized,  generalized,  and  continued,  though  the  two  latter 
forms  are  rare.  In  systematized  amnesia  the  memory  is  lost 
for  a  certain  category  of  ideas,  not  necessarily  acquired  at 
the  same  time,  but  relating  to  any  one  thing.  Thus  a  patient 
remembered  other  things,  but  forgot  all  circumstances  con- 
nected with  Janet's  personality.  In  local  amnesia  the  for- 
getfulness  is  for  certain  periods  of  time.  Thus,  in  traumatic 
hysteria,  the  patient  may  forget  circumstances  which  oc- 
curred immediately  before  or  immediately  after  the  accident, 
or  may  not  know  that  any  accident  occurred,  although  other- 
wise the  memory  remains  normal. 

Hysterical  affections  of  memory  are  inconstant  and  con- 
tradictory. They  are  not  necessarily  attended  with  deteri- 
oration of  reasoning  power.     In  traumatic  hysteria  a  frequent 


290  FUNCTIONAL   EFFECTS   OF   INJURY. 

form  of  memory  loss  is  due  to  lack  of  attention  and  is  con- 
fined to  recent  events.  The  patient  remembers  the  details 
of  the  experiences  of  childhood,  but  forgets  the  happenings 
of  yesterday. 

Aboulia,  or  impairment  of  will  power,  is  a  constant  men^ 
tal  symptom  of  the  disease  whatever  its  origin.  In  its  most 
common  form  it  is  manifested  by  a  difficulty  in  performing 
motor  or  intellectual  acts  at  will.  The  patient  feels  himself 
incapable  of  doing  the  simplest  things  or  of  undertaking- 
the  most  ordinary  intellectual  exercise.  Diminution  of  voli- 
tion is  particularly  frequent.  Instead  of  being  active  and' 
emotional,  the  patient  is  quiet  and  subdued.  There  is  hesi- 
tancy in  the  performance  of  voluntary  acts,  which  may 
amount  to  complete  loss  of  will  power.  Attempts  by  the 
physician  to  arouse  activity  of  mind  or  body  may  be  success- 
ful, but  the  patient  quickly  becomes  fatigued  and  confused 
and  inattentive. 

Some  of  the  more  striking  psychological  accidents,  such 
as  have  been  frequently  described  in  ordinary  h3'steria^ 
are  usually  wanting  in  traumatic  h3^steria.  Somnambulism, 
catalepsy,  and  the  like  are  rarely  mentioned  as  occurring  in. 
cases  which  arise  from  injury  or  fright. 

Yet,  although  the  occurrence  of  exaggerated  psychical 
disturbances  is  not  the  rule  when  the  psychosis  is  of  trau- 
matic origin,  they  are  sometimes  observed.  Laudun  has  de- 
scribed the  case  of — 

A  girl,  eleven  years  old,  who  was  very  much  frightened  while 
swinging.  Soon  afterward  she  had  several  attacks  of  coma  and 
paralysis,  with  cataleptic  flexibility  of  the  muscles.  In  the  first 
attack  the  pupils  were  widely  dilated,  and  did  not  respond  to  light. 
After  twenty-five  hours  the  patient  awoke  from  the  stupor,  but  the 
muscular  movements  remained  for  some  time  hesitating  and  slow. 
The  memory  for  the  time  which  elapsed  from  the  beginning  of 
the  attack  until  the  patient  awoke  was  entirely  lost.  The  suc- 
ceeding attacks,  of  which  there  were  several,  lasted  a  shorter 
time.     In  eight  days  the  patient  was  entirely  well  again.     During 


TRAUMATIC    HYSTERIA. 


291 


the  attacks  there  was  sugar  in  the  urine,  which  disappeared  when 
the  patient  recovered. 

The  general  appearance  and  manner  of  a  patient  suffer- 
ing from  traumatic  hysteria  are  the  results  of  the  mixture  of 
hysterical  and  neurasthenic  symptoms.  He  is  inattentive, 
inactive,  and  indifferent,  and  shows  a  diminution  of  interest 
in  his  surroundings.  He  is  credulous  and  may  seem  fond  of 
exaggeration  and  imposture,  but  his  credulity  is  childlike 
and  his  exaggeration  and  deception  lacks  the  cunning  of  the 
paranoiac.  He  is  often  pictured  as  a  partial  maniac,  ever 
ready  to  laugh  or  weep,  or  to  give  evidences  of  exalted  men- 
tal states.  As  a  matter  of  fact,  he  is  moody,  introspective, 
and  depressed,  approaching  the  type  of  melancholia  more 
closely  than  that  of  mania. 

Anaesthesia. — Hysterical  ansesthesia  is  a  symptom  of 
which  the  patient  only  rarely  complains,  and  of  which  he  is 
often  ignorant  until  its  existence  is  pointed  out  to  him  by 
medical  examination.  The  subjective  difference  between 
hysterical  ansesthesia  and  anaesthesia  of  organic  origin  is 
well  illustrated  by  a  case  related  by  Janet : 

A  young  girl  cut  her  right  wrist  with  a  piece  of  glass,  thus  in- 
juring the  median  nerve.  There  was  no  paralysis,  but  she  com- 
plained of  tingling  and  anaesthesia,  total  in  places,  over  the  palm 
of  the  hand  and  fingers.  The  physician  who  examined  the  case 
discovered  that  there  was  also  a  complete  left  hysterical  hemi- 
anaesthesia,  of  which  the  patient  not  only  did  not  complain,  but 
whose  existence  she  did  not  even  suspect.  There  could  be  no- 
more  convincing  proof  of  the  necessity  for  thorough  sensory  ex- 
amination in  nervous  cases. 

Ignorance  of  the  existence  of  hysterical  ansesthesia  on  the 
part  of  the  patient  is  an  ignorance  of  personality  only.  We 
have  seen  that  in  hysterical  ansesthesia,  sensations  are  really 
perceived,  although  they  do  not  enter  the  field  of  conscious- 
ness. This  fact  receives  additional  proof  by  the  absence  of 
any  injury  to  regions  which  are  hysterically  insensible.  It 
is  almost  unheard  of  for  a  hand,  the  seat  of  the  profoundest 


2Q2  FUNCTIONAL   EFFECTS   OF    INJURY. 

hysterical  ansesthesia,  to  be  injured  without  the  patient's 
knowledge,  by  cuts  or  burns.  This  is  in  direct  contrast  to 
the  anaesthesia  resulting  from  injury  to  the  peripheral 
nerves  or  spinal  cord,  for  when  complete  anaesthesia  of  the 
hand  is  of  organic  origin,  it  almost  invariably  happens  that 
the  patient  is  unconsciously  cut,  bruised,  or  burned. 

However,  in  spite  of  the  fact  that  until  told  of  it  the  pa- 
tients may  be  unaware  of  the  existence  of  aucesthesia,  loss  of 
some  form  of  sensibility  in  the  skin  or  mucous  membranes  is 
by  far  the  commonest  symptom  of  hysteria.  Even  in  Amer- 
ica, where  the  more  pronounced  hysterical  affections  are  in- 
frequent, hysterical  ansesthesia  is  constantly  met  with.  The 
ancesthesia  is  most  commonly  total,  all  forms  of  sensibility 
being  impaired  or  abolished.  Less  frequently  the  different 
sensations  may  be  dissociated.  This  dissociation  may  be 
similar  to  that  of  syringomyelia.  Thus,  of  seventeen  cases 
of  hysterical  hemi-thermo-ansesthesia  examined  by  Charcot, 
eleven  presented  the  type  of  total  anaesthesia.  In  six  there 
was  a  dissociation  of  sensations.  Two  of  these  six  had  loss 
of  temperature  sense,  with  preservation  of  sensibility  to 
touch  and  pain.  In  the  four  others  the  dissociation  was 
the  same  as  that  observed  in  syringomyelia — i.  e.,  touch 
sense  preserved,  pain  and  temperature  sense  lost.  Anal- 
gesia is  the  most  common  of  any  individual  sensory  defect. 

The  different  forms  of  sensibility  may  be  entirely  lost  or 
merely  impaired,  so  that  the  ordinary  stimuli  applied  to  the 
skin  or  mucous  membranes  pass  unperceived,  but  are  recog- 
nized when  the  irritation  is  intensified.  Thus,  in  hysterical 
impairment  of  touch  sense,  slight  touches  may  not  be  recog- 
nized, although  deep  pressure  is  felt ;  or  there  may  be  anal- 
gesia for  ordinary  painful  stimuli,  while  strong  electrical 
currents  can  not  be  well  borne. 

The  limits  of  cutaneous  anaesthesia,  in  my  experience, 
have  usually  been  sharply  defined.  The  commonest  topo- 
graphical distribution  of  hysterical  anaesthesia  is  unilateral. 


TRAUMATIC    HYSTERIA. 


293 


In  the  clinic  it  most  frequently  occurs  in  the  form  of  a  left 
hemianaesthesia  extending  from  the  head  to  the  feet,  and 
involving  the  mucous  membrane  of  the  eye  and  mouth  of 
the  affected  side  (Fig.  48).  In  traumatic  hysteria,  however, 
in  which  paralysis  is  so  frequent,  the  sensory  loss  commonly 


Pig.  48. — The  most  fre- 
quent distribution  of  hys- 
terical anaesthesia. 


Fig.  49. — Disseminated  anaesthesia. 
(After  Pitres. ) 


coincides  in  its  distribution  with  that  of  the  parts  paralyzed 
(morphological  anaesthesia,  see  Fig.  46).  If  there  is  hemi- 
plegia, there  will  be  hemianassthesia ;  if  paraplegia,  the  sen- 
sory loss  will  be  from  the  waist  down,  usually,  though  not 
always,  skipping  the  genital  organs.  If  muscular  power  is 
lost  in  one  limb  only,  the  anaesthesia  involves  the  skin  which 
covers  the  paralyzed  member.  When  the  sensory  changes 
occur  in  segments  of  limbs  only,  it  is  called  segmetal,  a  form 
which  is  frequently  seen  in  the  involvement  of  areas  of  skin 
ordinarily  covered  by  gloves  and  stockings  (glove  anesthe- 
sia— stocking  anaesthesia). 

Sensory  loss  may  occur  in  scattered  areas  (Fig.  49)  over 


294  FUNCTIONAL   EFFECTS   OF   INJURY. 

the  whole  body — a  form  easily  overlooked  if  sensory  exami- 
nation is  not  painstaking.  Pronounced  anaesthesia  of  the 
whole  cutaneous  surface  is  usually  associated  with  other 
unmistakable  hysterical  symptoms,  and  is  rarely  observed 
except  in  coma. 

The  topographical  distribution  of  hysterical  anaesthesia 
differs  essentially  from  that  due  to  other  causes.  It  never 
follows  the  distribution  of  individual  nerves.  In  trans- 
verse spinal-cord  lesions  the  resulting  loss  of  cutaneous 
sensibility  is  found  in  the  parts  supplied  by  the  injured  seg- 
ments ;  these  parts  do  not  correspond  to  the  areas  affected 
by  hysterical  ancesthesia.  Furthermore,  the  penis  usually 
retains  its  sensibility  in  hysteria,  but  never  does  in  lesions 
above  the  fifth  lumbar  segment.  In  unilateral  spinal-cord 
lesions  (Brown-Sequard  paralysis)  paralysis  of  motion  and 
sensation  are  on  opposite  sides.  The  topographical  distri- 
bution of  the  anaesthesia  of  syringomyelia  follows  the  spinal 
segmental  type.  In  organic  lesions  of  the  brain  the  result- 
ing ansesthesia  is  generally  slight,  and  the  associated  symp- 
toms are  usually  sufificient  to  permit  of  a  correct  diagnosis 
(see  page  60). 

Hysterical  angesthesia  ma}"  come  and  go,  be  permanent 
or  transitory,  or  may  frequently  change  its  situation.  It  or- 
dinarily disappears  during  sleep,  and  may  disappear  during 
the  various  intoxications.  Its  locality  can  frequently  be 
made  to  change  during  the  hypnotic  sleep,  and  suggestions 
received  during  waking  hours  may  cause  it  to  disappear  or 
to  assume  different  topographical  distributions. 

The  various  alterations  of  the  sensor}-  functions  of  the 
skin  and  mucous  membranes  which  take  place  after  the  hys- 
terical attack,  after  strong  emotions,  or  after  the  use  of  the 
magnet,  are  the  results  of  suggestion.  Most  of  the  psychia- 
trical clinics  of  Europe  are  supplied  with  huge  horseshoe 
magnets,  which  are  used  to  demonstrate  the  mobility  of 
hysterical  anaesthesia.     Since  Peterson  has  shown  that  there 


TRAUMATIC    HYSTERIA.  295 

are  absolutely  no  physiological  effects  from  the  strongest 
magnetic  currents,  it  is  an  inevitable  conclusion  that  the  so- 
called  magneto-therapy  acts  solely  by  mental  impressions. 

The  cutaneous  surface  is  the  most  frequent  seat  of  anaes- 
thesia. The  mucous  membranes,  especially  those  of  the  eye- 
lids and  pharynx,  the  muscles,  joints,  and  viscera,  are  also 
common  locations.  To  the  eye  and  to  the  touch,  hysteric- 
ally ansesthetic  skin  is  normal.  It  is  not  paler  than  normal 
skin,  but  for  some  unexplained  reason  it  has  a  diminished 
tendency  to  bleed  when  pricked.  In  the  anaesthetic  areas 
the  muscular  sense  is  regularly  abolished. 

Hyperaesthesia. — Hyperassthesia  is  a  sensory  symptom 
of  hysteria  for  which  examination  is  usually  unnecessary. 
The  patients  complain  of  spontaneous  pain  in  the  hyperaes- 
thetic  parts,  as  well  as  of  the  suffering  caused  by  slight  jars 
or  knocks.  The  pain  may  be  very  severe  and  lasting,  as  in 
the  hysterical  joint  affections,  or  it  may  be  transitory  and 
mobile,  like  hysterical  anaesthesia.  Hyperalgesia  is  more 
frequent  than  spontaneous  pain.  The  slightest  contact  may 
cause  expressions  of  agony,  and  the  patients  are  very  un- 
willing to  permit  any  touches  on  the  hypersensitive  parts. 
In  such  cases  deep  pressure  is  often  well  borne.  The  pain 
caused  by  touching  the  hypersensitive  part  is  much  accent- 
uated if  the  patient  knows  that  the  test  is  about  to  be  ap- 
plied. It  often  happens  that  no  pain  is  felt  when  the  part  is 
brushed  or  tapped  while  the  patient's  attention  is  fixed  on 
something  else. 

The  value  of  the  Mannkopff  sign  is  questionable  in  trau- 
matic hysteria. 

The  situation  of  hyperaesthesia  is  variable.  General  hy- 
peraesthesia is  extremely  rare.  Hemihyper^sthesia  may 
occur.  Ancesthetic  areas  frequently  contain  hyperaesthetic 
zones.  In  the  male  the  testicle,  and  in  the  female  the  ova- 
rian regions,  are  common  locations  of  hyperaesthesia.  In 
traumatic  hysteria  there  are  usually  areas  of  hyperaesthesia 


296  FUNCTIONAL   EFFECTS   OF   INJURY. 

which  correspond  in  situation  to  the  seat  of  the  injury. 
This  is  the  form  of  hypereesthesia  described  in  the  local 
traumatic  neurosis  of  Striimpell.  If  the  back  has  been 
twisted  or  injured  in  any  way,  there  is  often  the  pain  of 
traumatic  lumbago,  although  the  spinous  processes  of  cer- 
tain vertebrce  are  frequently  hypersensitive,  independent- 
ly of  lumbago.  The  clavus  hystericus — the  sensation  as 
though  a  nail  were  being  driven  into  the  head — is  a  hys- 
terical symptom  generally  familiar.  In  addition  to  these 
forms  of  increased  sensitiveness,  headache  and  peculiar  sen- 
sations in  the  head  are  common.  In  paroxysmal  hysteria 
the  areas  of  hypercesthesia  become  hysterogenetic  zones — 
that  is,  pressure  upon  them  may  induce  a  paroxysm,  or 
pressure  exerted  during  a  paroxysm  may  cause  it  to  cease. 

Hysterical  pain  does  not  usually  interfere  with  sleep,  nor 
is  it  accompanied  with  the  nutritional  disturbances  which 
are  such  common  consequences  of  pain  from  other  causes. 
It  is  a  difficult  symptom  to  explain.  Janet  suggests  that  it 
is  entirely  due  to  the  ideas  aroused  by  association  relative  to 
contact.  Although,  psychologically,  the  pain  is  probably 
not  genuine,  it  is  real  to  the  patient,  and  may  cause  him 
much  discomfort  and  suffering. 

Special  Senses. 

Vision. — Next  to  cutaneous  anaesthesia,  disturbances  of 
vision  are  the  most  frequent  of  the  hysterical  stigmata. 
Apart  from  any  possible  pre-existing  organic  defects  or  dis- 
ease, the  eye  is  found  to  be  anatomically  normal.  The  con- 
junctivae are  very  constantly  angesthetic,  and  the  palpebro- 
conjunctival  reflex  is  usually  abolished.  Examination  of  the 
pupils,  of  the  optic  nerves,  of  the  ocular  muscles,  and  of 
the  refracting  apparatus,  is,  with  few  exceptions,  negative. 
Nevertheless,  vision  may  be  impaired  (amblyopia),  or  there 
may  be  complete  blindness  of  one  eye  (amaurosis).     Bilat- 


TRAUMATIC    HYSTERIA. 


297 


eral  hysterical  amaurosis,  on  the  other  hand,  is  one  of  the 
rarest  of  hysterical  symptoms. 

When  the  eyes  are  examined  with  the  perimeter,  it  is 
found  that  there  is  a  peripheral  limitation  of  the  fields. 

In  the  larger  number  of  cases  of  hysterical  amblyopia 
the  peripheral  limitation  is  slight,  not  exceeding  ten  or 
fifteen  degrees.  In  some  cases,  however,  it  may  be  very 
extensive,  the  perimeter  showing  that  only  a  few  degrees  of 


L.^ 


RE. 


Fig.  50. — Extreme  concentric  contraction  of  the  visual  fields. 
(After  Gilles  de  la  Tourette.) 


the  field  retain  their  normal  seeing  power.  When  slight  in 
degree,  the  contraction  most  commonly  follows  the  pe- 
riphery of  the  normal  field,  but  when  it  is  excessive  it  is 
concentric  (Fig.  50).  Both  eyes  usually  share  in  the  visual 
impairment,  though  it  is  customarily  more  marked  in  one 
eye  than  in  the  other.  If  there  is  unilateral  paralysis 
or  unilateral  cutaneous  anaesthesia  of  the  body,  the  more 
affected  eye  will  correspond  to  the  paralyzed  or  angesthetic 
side.  At  different  examinations,  the  extent  of  vision  often 
varies,  but  the  variation  does  not  follow  the  regular  shifting 


2Qg  FUNCTIONAL    EFFECTS    OF    INJURY. 

type  observed  in  neurasthenia.  Several  examinations  are 
advisable,  and  they  should  be  conducted  with  a  view  to 
rapidity,  rather  than  to  minute  accuracy.  Since  the  field 
often  changes  as  the  result  of  any  of  the  various  hysterical 
accidents,  or  with  the  general  condition  of  the  patient,  it 
has  been  called  by  Janet  the  "  barometer  of  hysteria." 

Frequently  associated  with  this  limitation  of  vision  for 
form  are  characteristic  abnormities  in  the  color  fields. 
With  contraction  of  the  visual  field  for  form,  the  perception 
of  the  most  internal  colors  may  be  lost,  or  w^hen  the  con- 
traction for  form  is  only  moderate  in  degree  there  may  be  a 
reversal  of  the  normal  color  fields  ;  thus  red  is  often  seen  in 
a  larger  field  than  blue. 

Visual  disturbances,  like  those  of  general  sensation,  are 
frequently  discoveries  of  the  examining  room.  The  acuity 
of  central  vision  ordinarily  remains  unimpaired.  Subjective 
ocular  disturbances,  such  as  flashes  of  light  before  the  eyes, 
muscse  volitantes,  etc.,  occur,  but  the  patients  often  neither 
complain  nor  are  conscious  of  any  trouble  wath  sight,  and 
they  are  not  subject  to  the  disabilities  resulting  from  con- 
traction of  the  visual  field  which  are  present  when  it  occurs 
from  organic  causes.  Hysterical  patients  in  reality  see,  al- 
though visual  perception  does  not  become  known  to  the 
higher  consciousness.  Thus  hysterical  amblyopia,  like  other 
hysterical  symptoms,  is  actually  false,  although,  when  the 
patient  is  conscious  of  it,  it  is  real  to  him. 

Although  the  patient  may  be  unconscious  of  any  visual 
disturbances,  examination  of  the  seeing  power  made  of  each 
eye  separately  may  show  that  in  one  eye  vision  is  impaired 
or  lost.  While  it  seems  almost  incredible  that  any  one  can 
be  totally  blind  in  one  eye  without  knowing  it,  examination 
of  many  cases  has  shown  that  unilateral  hysterical  amaurosis 
may  exist  independently  of  the  patient's  knowledge.  That 
the  apparently  contradictory  manifestations  of  hysterical 
amblyopia  may  be  genuine  and  exist,  when  the  patient  has 


TRAUMATIC    HYSTERIA. 


299 


no  motive  to  deceive  or  to  be  "  suggested,"  has  been  proved 
with  certainty  by  Prince.  He  recently  examined  a  case  in 
which,  instead  of  there  being  anything  to  be  gained  by  simula- 
tion, there  were  the  strongest  reasons  why  the  patient  should 
appear  sound  in  every  way,  for  he  was  a  very  zealous  appli- 
cant for  a  position  on  the  Boston  police  force.  The  ocular 
symptoms,  together  with  other  hysterical  stigmata,  w^ere  dis- 
covered at  the  time  of  his  medical  examination  for  admission. 

Prince  also  reports  unusual  symptoms  in  a  man  who,  as  the  re- 
sult of  an  accident  on  an  electric  street  car,  developed  hysterical 
hemiplegia  and  hemianesthesia  and  ocular  symptoms.  Vision  in 
the  right  eye  was  good,  but  on  the  left  side  (the  hemiplegic  side) 
there  were  amblyopia,  color  blindness,  contraction  of  the  field  of 
vision,  polyopia,  a  retraction  of  the  near  point,  and  an  approach  of 
the  far  point  to  a  distance  of  about  eight  feet. 

The  visual  disturbances  were  noticed  only  when  the  right 
(sound)  eye  was  closed. 

Disorders  of  the  other  special  senses  are  less  frequent. 
If  there  is  impairment  of  hearing  it  is  almost  always  uni- 
lateral, corresponding  to  the  anaesthetic  side  of  the  body. 
Bone  conduction  is  interfered  with  in  such  cases.  Loss  of 
^mell  or  taste  may  be  bilateral,  and  is  usually  associated 
with  angesthesia  of  the  nasal  mucous  membranes  and  of  the 
inner  surface  of  the  lips  and  of  the  tongue.  Impairment  of 
these  functions  is  found  under  circumstances  similar  to 
those  associated  with  anaesthesia  occurring  elsewhere. 

In  a  recent  Vanderbilt  Clinic  case,  as  a  result  of  a  bicycle  acci- 
dent, a  young  man  lost  for  several  months  the  senses  of  smell  and 
taste.  This  case  is  particularly  remarkable  as  none  of  the  more 
common  hysterical  stigmata  were  present.  The  visual  fields  were 
not  contracted,  the  cutaneous  sensibility  was  normal,  and  there 
were  no  paralyses.  Inasmuch,  however,  as  there  had  been  no 
injury  to  the  mouth  or  pharynx,  or  other  gross  injuries,  we  were 
•obliged  to  consider  the  ageusia  and  the  anosmia  as  functional. 

Hypergesthesia  of  hearing,  smell,  or  taste  may  also  occur, 
and  is  evidenced  by  subjective  disturbances  of  function  of 
these  senses. 


300  functional  effects  of  injury. 

Motor  Symptoms, 

Paralysis. — Paralysis  is  an  hysterical  accident  rather  than* 
a  permanent  stigma  of  the  disease.  Slight  injuries  frequently 
produce  marked  local  symptoms  in  persons  who  are  already 
affected  by  the  disorder,  or,  as  we  have  seen  in  discussing 
the  aetiology  of  hysteria,  the  psychosis  may  appear  for  the 
first  time  after  any  accident  in  which  the  factors  of  fright, 
and  injury  are  prominent. 

In  the  larger  number  of  cases  of  traumatic  hysteria  the 
local  injury  is  trifling,  or  at  best  not  severe.  Hysterical  pa- 
ralysis may,  of  course,  follow  grave  injuries ;  but  clinical 
experience  shows  that  the  trauma  itself  plays  only  a  subor-^ 
dinate  part.  The  loss  of  muscular  power  is  particularly 
prone  to  follow  accidents  in  which  the  emotions  have  been 
actively  called  into  play.  This  is  the  "traumatic  sugges- 
tion "  of  Charcot.  Ordinarily  there  is  some  little  interval  of 
time  between  the  occurrence  of  the  accident  and  the  appear- 
ance of  the  paralysis.  During  this  "period  of  meditation" 
the  patient  reflects  upon  his  injury,  and,  through  pain  or  dis- 
comfort, his  attention  is  directed  to  the  injured  part  until 
gradually  or  suddenly  the  power  of  voluntary  motion  in  it 
becomes  impaired  or  lost.  The  sudden  paral3'Sis  of  trau- 
matic hysteria  is  rarely  accompanied  by  the  associated  signs 
of  paralysis  due  to  organic  lesions  of  the  brain  or  spinal  cord. 
Unless  developed  during  an  hysterical  seizure,  or  unless  the 
shock  is  extreme,  there  is  no  prolonged  loss  of  consciousness. 

When  there  is  loss  of  power  in  a  limb,  usually  some  of  the 
muscles  escape,  although  all  may.  be  paralyzed.  It  some- 
times happens  that  the  paralysis  affects  certain  muscular 
functions  only,  and  that  the  pseudo-paralyzed  muscles  can 
perform  other  movements  perfectly  well.  This  is  well  illus- 
trated by  the  condition  first  described  by  Blocq,  under  the 
name  of  astasia-abasia.  In  this  condition  the  patient  has  en- 
tire use  of  the  legs  for  all  movements  except  those  necessary 


TRAUMATIC    HYSTERIA.  ^OI 

for  Standing-  or  walking.  He  may  be  able  to  move  the  legs 
in  bed,  or  to  dance,  or  to  hold  himself  on  the  toes,  while  all 
attempts  at  standing  or  walking  prove  ineffectual.  On  at- 
tempting them  the  patient  falls  immediately  to  the  floor. 
This  condition  differs  from  most  forms  of  hysterical  paral}^- 
sis  in  that  there  is  no  anaesthesia. 

The  possible  medico-legal  importance  of  astasia-abasia 
has  been  shown  by  Bremer  : 

A  woman,  forty-nine  years  of  age,  married,  claimed  that  she 
had  become  paralyzed  as  a  result  of  injuries  received  in  an  elevator. 
She  asserted  that  by  a  sudden  stopping  of  the  elevator  she  had 
been  thrown  forward  from  the  seat,  striking  her  head,  and  that 
since  that  time  her  lower  extremities  were  paralyzed.  She 
brought  suit  for  twenty  thousand  dollars.  The  physicians  who 
appeared  on  behalf  of  the  plaintiff  admitted  that  there  were  no  in- 
terference with  the  functions  of  the  bladder  or  rectum,  or  loss  of 
sensation  ;  but  they  asserted  that  while  the  patient  was  capable 
of  moving  her  legs  in  every  direction,  and  with  apparently  normal 
strength  in  the  sitting  or  lying  position,  she  was  not  able  to  either 
stand  or  walk.  The  expert  for  the  defense  accepted  the  symp- 
toms as  described  by  the  plaintiff's  physicians.  But  instead  of 
attributing  this  peculiar  form  of  paralysis  to  an  injury  to  the 
spinal  cord,  he  ascribed  to  it  only  such  importance  as  belongs  to 
hysteria.  It  was  then  shown  that  the  woman  had  had  previous 
hysterical  accidents,  and  that  the  astasia-abasia  was  only  a  new 
symptom  of  the  hysteria  from  which  she  had  been  suffering  for 
years.  The  jury  adopted  the  views  of  the  expert  for  the  defense, 
and  gave  a  verdict  favorable  to  the  defendant. 

The  degree  of  hysterical  paral3'sis  varies.  It  may  amount 
to  nothing  more  than  weakness  which  is  universally  distrib- 
uted, a  condition  to  which  Charcot  gave  the  name  of  aniyos- 
thcnia. 

Amyosthenia,  however,  is  a  permanent  stigma  rather  than 
a  hysterical  accident.  It  is  manifested  by  general  muscular 
weakness,  such  as  is  seen  in  neurasthenia,  but,  unlike  neuras- 
thenic weakness,  it  is  apparent  only.  In  hysterical  paralysis, 
the  patients  in  reality  retain  their  muscular  power,  as  may 


002  FUNCTIONAL   EFFECTS   OF    INJURY. 

be  proved  by  the  muscular  work  they  do.  It  is  when  their 
attention  is  drawn  to  the  movements  they  are  about  to  per- 
form— as  in  dynamometric  tests,  or  in  performing  move- 
ments at  command  —  that  the  weakness  is  chiefly  mani- 
fested. "  It  sounds  like  '  I  will  not,'  but  it  really  is  '  I  can 
not  will.'  " 

The  degree  of  paralysis  varies  also  at  different  times,  be- 
ing more  marked  at  one  examination  than  at  another.  As 
long  as  the  disease  remains  active  the  loss  of  power  usually 
becomes  progressively  greater.  Electrical  reactions  in  the 
paralyzed  muscles  almost  always  remain  normal,  although  a 
few  cases  with  diminished  electrical  excitability  have  been 
recorded.  Atrophy  is  rarely  present,  and  never  reaches  an 
extreme  degree. 

The  most  common  forms  of  hysterical  paralj^sis  are  hemi- 
plegia, brachial  monoplegia,  and  paraplegia. 

Hemiplegia  occurs  most  frequently  on  the  left  side.  It 
has  many  points  of  difference  from  organic  hemiplegia — viz., 
the  face  is  practically  never  paralyzed,  although  there  may 
be  an  associated  spasm  of  the  facial  muscles,  the  leg  is  more 
involved  than  the  arm,  the  knee-jerks  are  not  morbidly  exag 
gerated,  and  foot  clonus  is  absent,  except  in  some  cases  in 
which  the  foot  is  contracted  in  extension.  In  organic  spastic 
hemiplegia  the  mowing  gait  is  a  sign  which  the  most  inexpe- 
rienced may  interpret.  The  leg  is  circumducted  in  a  very 
characteristic  way.  Even  in  flaccid  hemiplegia,  if  the  pa- 
tient can  walk  at  all,  some  use  is  made  of  the  paralyzed  leg. 
But  in  hysterical  paralysis  the  leg  is  dragged  as  though  it 
were  an  inert  mass.  This  difference  is  well  seen  in  the  ac- 
companying reproduction  of  footprints  (Fig.  5 1).  In  organic 
hemiplegia,  anaesthesia  is  rarely  an  important  symptom  (see 
page  60),  while  the  anaesthesia  of  hysterical  hemiplegia  is 
pronounced,  involving  the  whole  of  the  paralyzed  half  of  the 
body  and  usually  associated  with  anaesthesia  of  the  special 
sense  organs. 


TRAUMATIC    HYSTERIA. 


30; 


% 


r  % 


^ 


^ 


Monoplegia  is  perhaps  the  most  frequent  form  of  pa- 
ralysis observed  in  traumatic  hysteria.      The  left  side  is  the 
one  usually  affected.      The  loss  of  power  may  involve  the 
whole  limb,  or,  as  is  more  frequent,  only  certain  segments 
or  muscles  are  paralyzed.     The 
arm    is    much    oftener    involved 
than  the  leg;  it  may  hang  down 
from    the    shoulder   as    an    inert 
mass,     or     the     shoulder     may 
escape,  and  only  the  movements 
of  the  hands  be  impaired  or  lost. 
The  symptomatology  of  hysteri- 
cal brachial  monoplegia  has  been 
established  through  the  work  of 
Miura,    who   studied    thirty-one 
cases    in    which    this    condition 
was  a  symptom.      In  fifteen  the 
paralysis   was   of   traumatic  ori- 
gin,   and    followed    the     injury 
immediately,    or   was    separated 
from    it   by  a  "  meditative "  pe- 
riod.    The  extent  of  the  motor 
loss   varied    from    weakness    of 
wrist   and    fingers   to    complete 
paralysis     of     the     whole     arm. 
When   weakness  of  the  leg  was 
added  to  the  brachial  monople- 
gia there  was  an  associated  hemianaesthesia.     In  nine  cases 
there  was  hemianaesthesia  with  pure   brachial  monoplegia. 
In  other  cases  the  anaesthesia  was  limited  to  the  paralyzed 
arm,  so  that  it  was  bounded  superiorly   by  a  line  perpen- 
dicular to  the  long  axis  of  the  extremity.     In  one  case  there 
was  no  anaesthesia  at  all. 

The  following  case,  reported  by  Lebrun,  is  interesting,  as 
it  shows  both  the  possibility  of  hysterical  monoplegia  devel- 


1 


Fig.  51. — Impressions  which  illustrate 
the  differences  in  the  gait  (1  and  2) 
of  hysterical  hemiplegia,  and  (3) 
organic  hemiplegia  of  the  flaccid 
type.  (From  Blocq,  after  Gilles 
de  la  Tourette.) 


,04  FUNCTIONAL  EFFECTS  OF  INJURY. 

oping  from  slight  injury,  and  the  occurrence  of  convulsive 
attacks  as  a  conaplication  : 

A  young  man,  eighteen  and  a  half  years  of  age,  when  examined 
for  miUtary  service,  was  found  sound  in  every  way  and  was  enhsted. 
A  few,  weeks  later,  while  being  vaccinated,  he  was  accidentally 
pricked  by  the  lancet  on  the  left  elbow.  He  fell  unconscious 
almost  immediately,  and  on  the  succeeding  day  had  several  more 
attacks  of  unconsciousness.  In  a  few  days  after  the  injury,  which 
was  obviously  very  trifling,  power  in  the  left  arm  began  to  fail. 
He  was  released  from  duty,  and,  as  he  was  becoming  worse,  he 
voluntarily  sought  the  hospital,  where  he  was  seen  by  Lebrun,  who 
made  the  following  notes  : 

"Drooping  of  left  shoulder.  The  left  arm  hangs  inert ;  when 
told  to  move  it,  the  patient  lifts  it  a  little,  with  effort,  but  lets  it 
fall  again.  He  can  hold  nothing  in  the  hand.  Electrical  reaction 
normal.  No  atrophy.  Total  anesthesia  of  the  left  arm,  extending 
superiorly  a  little  above  the  shoulder.  There  is  a  concentric  Hmita- 
tion  of  the  visual  fields,  most  marked  on  the  left  side.  The  testi- 
cles are  hysterogenetic  zones.  The  attacks  are  ushered  in  by  vio- 
lent headache,  buzzing  in  the  ears  and  throbbing  of  the  temples, 
and  by  the  globus  hystericus.  The  face  becomes  congested  and 
anxious  in  appearance.  Inspiration  is  prolonged  and  difficult. 
Expiration  is  short.  This,  the  first  period  of  the  attack,  lasts 
about  one  minute.  It  is  followed  by  clonic  spasms,  the  arc  en 
cercle  and  other  histrionic  attitudes  and  movements.  This  period 
closes  by  the  patient  bursting  into  tears.  In  these  attacks  con- 
sciousness was  only  partially  lost.  The  patient  understood  what 
was  going  on  around  him,  but  could  not  reply." 

This  patient  was  apparently  a  confirmed  hysteric,  since  he  had 
been  paraplegic  in  childhood  as  the  result  of  a  slight  injury,  and 
had  always  been  suggestible.  In  his  case  the  slight  injury  caused 
by  the  lancet  was  sufficient  to  call  into  action  the  dormant  psy- 
chosis. 

Although  the  arm  is  by  far  the  most  frequent  situation  of 
hysterical  monoplegia,  other  parts  may  be  the  seat  of  local- 
ized paralysis.  Hysterical  monoplegia  of  the  leg  is  not 
rare.  Also  a  few  cases  of  hysterical  paralysis,  with  anes- 
thesia, limited  to  the  one  side  of  the  face,  have  been  ob- 
served. 


TRAUMATIC    HYSTERIA.  305 

Paraplegia. — When  hysterical  paraplegia  results  from 
injury  or  shock,  its  onset  is  usually  sudden.  It  is  particularly 
liable  to  be  complicated  by  the  development  of  contractures, 
which  may  be  permanent.  The  loss  of  power  may  involve 
the  whole  of  both  limbs,  rendering  all  motion  impossible, 
although  more  commonly  some  motor  power  is  retained,  so 
that  the  legs  or  feet  may  be  moved  about  in  bed. 

The  reflexes  are  unchanged,  except  the  plantar  reflexes, 
which  are  frequently  lost.  Gilles  de  la  Tourette  says  that 
incontinence  of  urine  and  feeces  may  occur.  This  is  certainly 
very  unusual.  Ordinarily  the  patients  retain  perfect  control 
of  these  functions.  If  control  is  lost,  the  presumption  of 
organic  mischief  becomes  very  strong. 

The  anesthesia  in  hysterical  paraplegia  usually  extends 
from  the  waist  downward,  involving  all  parts  except  the 
genital  organs.  This  rule  is  not  invariable,  for  the  genital 
organs  may  be  hypersesthetic  or  anaesthetic,  or  other  parts 
may  retain  their  sensibility.  A  case  detailed  by  Souques 
illustrates  this : 

A  man,  twenty-nine  years  of  age,  without  discoverable  nerv- 
ous taint,  was  very  much  frightened  and  then  knocked  down,  by  a 
horse.  He  was  thrown  against  the  curbstone,  thus  receiving  a 
contusion  of  the  hip,  and  immediately  went  into  coma  which  lasted 
two  days.  In  eight  days  he  was  able  to  walk  with  difficulty,  but 
soon  went  into  coma  again,  which  lasted  this  time  five  days.  He 
lost  for  a  time  the  power  of  speech.  Then  he  began  to  have 
nightmares  and  hallucinations  relative  to  the  accident. 

Physical  examination  at  this  time  showed  complete  anaesthesia 
(Fig.  52)  below  the  waist,  with  the  exception  that  there  was  only 
a  diminution  of  sensibility  of  the  genital  organs,  and  parts  of 
both  feet  were  normally  sensitive.  The  muscular  sense  was  lost. 
Movement  was  almost  entirely  abolished  in  the  lower  extremities. 
The  patient  was  unable  to  flex  the  thigh  or  lift  the  heel  from 
the  bed;  but  he  could  be  seen  to  attempt  these  movements,  and 
the  muscles  also  could  be  seen  to  contract.  Slight  power  of  flexion 
and  extension  persisted  in  the  toes.  There  was  absolutely  no  re- 
sistance to  passive  movement.  The  knee-jerks  were  diminished 
but  present  on  both  sides.     The  scalp  was  hypersesthetic.     Left 


3o6 


FUNCTIONAL   EFFECTS   OF    INJURY. 


glosso-labio  hemispasm.  The  superior  extremities  were  weak,  but 
all  movements  in  them  possible.  Slight  tremor.  Limitation  of  the 
visual  fields.  Loss  of  the  sense  of  smell  on  the  right  side  ;  the 
sense  of  taste  abolished  on  both  sides.  While  under  observa- 
tion this  patient  had  an  attack  of  mutism  and  dyspnoea. 


Fig.  52. — Anesthesia  in  a  case  of  hysterical  paraplegia.     (Souques.) 


Polyplegia. — Hysterical  paralysis  of  all  four  extremities 
is  unusual,  but  sometimes  occurs. 

Serieux  reports  the  case  of  a  young  girl,  fifteen  years  of  age, 
who,  after  a  severe  fright,  fell  into  convulsions  and  hallucinatory 
delirium,  during  which  her  arms  and  legs  received  slight  bruises. 
A  few  days  later  all  four  extremities  became  paralyzed,  the  de- 
gree of  the  loss  of  muscular  power  in  any  limb  being  proportion- 
ate to  the  severity  of  the  injuries  the  limb  had  received  during  the 
convulsive  attacks.  The  paralysis  was  flaccid  and  there  was  a 
diminution  of  electrical  reactions  and  of  tendon  reflexes.  The 
muscles  were  the  seats  of  quick,  shocklike  contractions,  resem- 
bling those  of  electric  chorea.  Anesthesia  was  at  first  generally 
distributed,  but  was  very  variable.  The  visual  fields  were  con- 
tracted, and  the  smell  and  taste  were  lost. 

The  symptoms  eventually  passed  away,  except  a  left  hemi- 
ansesthesia. 


TRAUMATIC    HYSTERIA. 


307 


In  parts  which  are  the  seat  of  hysterical  paralysis  or 
anaesthesia  the  muscular  sense  is  lost,  as  may  be  demon- 
strated for  individual  limbs  by  the  ordinary  clinical  tests. 
Unsteadiness  of  standing  or  walking  is  sometimes  apparent 
at  once.  This  may  take  the  form  of  ataxic  movements  of 
the  leg,  such  as  occur  in  locomotor  ataxia.  The  ataxia  may 
be  more,  or  less  pronounced  than  in  tabes.  On  standing 
still  with  the  eyes  closed,  there  may  be  considerable  sway- 
ing of  the  body.  Some  hysterical  patients  can  not  stand  at 
all  with  closed  eyes.  In  a  recent  case  at  the  Vanderbilt 
Clinic  the  ataxia  was  most  marked  when  the  patient  tried  to 
get  up  from  a  chair.  These  disorders  of  movement  may 
occur  independently  of  paralysis.  The  ataxic  and  inco- 
ordinated  movements  seen  in  hysteria  often  obscure  the 
diagnosis,  and  render  a  proper  comprehension  of  the  case 
impossible  until  examination  has  shown  the  evidences  of 
organic  disease  to  be  absent,  or  has  revealed  the  presence  of 
some  of  the  hysterical  stigmata. 

Thus,  in  a  recent  Vanderbilt  Clinic  case,  the  patient's  chief 
complaint  was  of  an  inability  to  button  his  clothes.  The  move- 
ments of  the  fingers  were  uncertain  and  ataxic,  resembling  in  this 
respect  the  inco-ordination  seen  in  general  paresis.  These  symp- 
toms had  occurred  subsequently  to  a  fall  from  a  horse  car.  Ex- 
amination failed  to  reveal  any  paralysis  or  other  evidences  of 
organic. disease,  but  the  mental  condition  of  the  patient  was  char- 
acteristic of  traumatic  hysteria,  and  there  was  a  generalized  blunt- 
ing of  cutaneous  sensibility,  which  in  both  hands  and  over  the  left 
side  of  the  body  was  very  pronounced. 

Similarly,  an  active  farmer,  fifty-five  years  of  age,  was  thrown 
from  a  trolley  car,  and  soon  afterward  became  depressed,  apa- 
thetic, and  emotional.  A  suit  for  a  large  sum  was  brought  against 
the  company.  My  examination  showed  a  left  hemianfesthesia, 
weakness  in  the  muscles  of  the  left  side,  diminution  of  the  visual 
field,  and  similar  manifestations  of  hysteria.  There  were  no  evi- 
dences of  structural  lesion.  Uncertainty  in  movements  of  the 
legs  was  very  marked.  The  man  could  not,  apparently,  walk 
straight,  but  would  stagger  to  the  right.  On  standing  with  closed 
eyes  he  would  fall  toward  the  right,  although  he  never  let  himself 


3o8  FUNCTIONAL   EFFECTS   OF    INJURY. 

go  entirely.  His  wife  said  she  had  observed  him  when  he  was 
working  in  the  field,  and  that  he  would  then  stagger  to  the  right, 
though  he  never  fell. 

Contractures. — In  hysteria,  tonic  and  continued  spasm 
may  occur  in  almost  any  of  the  muscles,  but  is  most  frequent 
in  the  muscles  of  the  extremities.  The  contracture  may  de- 
velop suddenly  as  the  result  of  any  provoking  agent,  but 
usually  it  comes  slowly,  becoming  gradually  more  and  more 
extensive  and  severe.  It  may  complicate  paralysis,  espe- 
cially paraplegia,  or  may  occur  when  there  is  no  loss  of 
power  except  such  as  is  imposed  by  the  rigidity  of  the  mus- 
cles. Hysterical  contracture  may  so  closely  simulate  the 
contractures  due  to  degeneration  of  the  pyramidal  tracts 
that  it  is  sometimes  impossible,  from  morphological  appear- 
ances alone,  to  distinguish  between  the  two  conditions. 
The  state  of  the  muscles  themselves,  however,  is  very  differ- 
ent in  the  two  conditions.  In  hemiplegia,  or  in  disease  of  the 
spinal  cord,  the  contractures  come  on  gradually  ;  it  is  many 
weeks  before  they  are  very  pronounced,  and  even  then  they 
can  be  overcome  by  moderate  force.  It  is  common  in  neu- 
rological wards  to  see  a  hemiplegiac  straightening  out  the 
fingers  of  his  paralyzed  and  contracted  hand  ;  but  in  hyste- 
ria the  contractures  are  vise-like,  not  to  be  overcome  by  any 
moderate  degree  of  violence.  Both  sets  of  muscles  sur- 
rounding a  joint  may  be  so  tense  that  the  joint  is  held  abso- 
lutely motionless.  Also,  in  organic  injury  to  the  pyramidal 
tract,  increase  of  tendon-reflex  activity,  with  ankle  clonus, 
is  the  rule,  and  often  occurs,  soon  after  the  accident,  on 
the  unparalyzed  as  well  as  on  the  paralyzed  side.  On  the 
other  hand,  there  is  rarely  any  great  exaggeration  of  the 
tendon  reflexes  in  hysteria.  A  still  more  valuable  sign 
for  differential  diagnosis  is,  that  hysterical  contracture 
may  appear  after  injuries  too  trifling  to  induce  any  mor- 
bid conditions  of  organic  character.  The  appearance  of 
this  form  of  immobility  after  a  slight  injury  in  a  strong  and 


TRAUMATIC    HYSTERIA. 


309 


Fig.  53. — Hysterical  contracture. 
(After  Richer  and  Berbez.) 


apparently  healthy  man  is  well  shown  by  a  case  of  Berbez 
(Obs.  9) : 

The  patient  was  a  robust  blacksmith,  thirty-four  years  of  age, 
the  father  of  four  children.  The  man  had  always  been  appar- 
ently in  perfect  health.  He  denied  all  history  of  ancestral  or  per- 
sonal nervous  stigmata.  While  at  work  he  was  slightly  burned  on 
the  left  hand  and 
forearm  by  a  red-hot 
iron.  The  wound 
was  not  deep,  but 
took  six  weeks  to 
heal,  and  left  a  scar 
ten  or  twelve  centi- 
metres long  and  three 
or  four  centimetres 
wide,  on  the  back  of 
the  hand  and  lower  part  of  the  forearm.  There  was  no  par- 
ticular fright  connected  with  the  accident,  but  three  or  four  days 
later  the  patient  found  that  the  fingers  of  the  left  hand  M'ere  get- 
ting stiff  and  beginning  to  feel  numb.  This  condition  of  stiffness 
and  numbness  continued  for  seven  weeks,  when,  on  arising  one 
morning  after  a  rather  sleepless  night,  the  patient  found  his  hand 
in  the  attitude  of  main  en  griffe.  This  position  was  gradually 
changed  into  one  of  flexion  of  the  wrist  and  fingers,  with  prona- 
tion of  the  forearm  (Fig.  53). 

The  shoulder  and  upper  arm  were  not  involved ;  the  forearm 
was  pronated.  The  hand  was  flexed  on  the  forearm;  the  four 
fingers  were  so  tightly  flexed  that  the  nails  dug  into  the  palm  of 
the  hand.  The  fingers  were  tightly  pressed  together,  and  the 
thumb  was  firmly  fixed  on  the  external  surface  of  the  second  pha- 
lanx of  the  index  finger.  The  contractions,  which  persisted  at 
night,  were  so  pronounced  that  all  efforts  at  reduction  were  un- 
successful. Hysterical  stigmata  were  eventually  added  to  these 
symptoms.  The  left  side  of  the  body  became  the  seat  of  a  hemi- 
anaesthesia,  and  the  taste,  smell,  and  hearing  were  much  blunted 
on  the  left  side.  Both  visual  fields  were  contracted,  but  most 
markedly  on  the  left  side.  The  color  fields  were,  however,  not 
reversed. 

At  first,  magneto-therapy  was  able  to  induce  a  return  of  cuta- 
neous sensibility  to  all  of  the  left  side  except  the  parts  involved  in 
the  contracture.      They  remained  anaesthetic.      A  later   attempt 


3IO  FUNCTIONAL   EFFECTS   OF   INJURY. 

caused  the  sensibility  to  return  to  the  left  hand  and  arm,  but  was. 
followed  by  a  contracture  of  the  sound  (right)  hand. 

Hysterical  contractures  may  exist  only  for  a  short  time 
and  disappear  suddenly,  or  they  may  be  persistent  and  some- 
times they  are  permanent.  They  do  not  relax  during  sleep,, 
though  they  may  often  be  made  to  do  so  by  suggestion,  and 
almost  always  disappear  during  ether  narcosis.  When 
affecting  the  arms  or  legs  they  usually  assume  forms  dif- 
ferent from  those  of  organic  contractures.  In  a  common 
type  of  contracture  of  the  arm,  when  either  the  arm  alone 
or  the  arm  and  leg  are  both  involved,  the  arm  is  drawn 
across  the  chest,  the  forearm  is  partly  flexed,  the  wrist  is 
flexed,  and  the  fingers  are  tightly  closed  in  the  hand.  The 
hand  may  assume  various  positions  from  the  preponderance 
of  the  contracture  in  certain  muscles.  The  position  for 
holding  the  pen,  due  to  spasm  in  the  interossei,  is  not  un- 
usual. 

When  contracture  affects  the  lower  extremities,  they  are 
usually  held  absolutely  immobile  and  straight.  Not  uncom- 
monly a  contraction  of  the  calf  muscles  produces  a  condition 
of  equino-varus  with  flexion  of  the  toes. 

Although  in  paraplegia  the  legs  are  most  frequently  held 
in  rigid  extension  and  adduction,  they  may  assume  the  same 
type  of  flexion  as  is  seen  in  organic  disease  of  the  spinal 
cord. 

In  some  cases  the  diagnosis  of  hysterical  contracture  is. 
very  puzzling,  although  it  may  usually  be  made  by  examin- 
ing the  reflexes  (if  the  contractures  do  not  make  this  impos- 
sible), the  condition  of  the  muscles  therfiselves,  and  by  look- 
ing for  other  associated  signs  of  hysteria. 

Local  and  persistent  spasms  may  occur  in  individual  mus- 
cles or  muscle  groups.  The  extrinsic  eye  muscles  may  be 
involved.  Hysterical  blepharospasm,  which  is  not  infre- 
quent, may  be  unilateral  or  occur  on  both  sides.  It  gives  the 
appearance  of  ptosis.    Spasm  of  the  muscles  of  the  eyeball  is- 


TRAUMATIC    HYSTERIA.  ojj 

less  frequent.  One  side  of  the  face  may  be  the  seat  of  spasm, 
giving  rise  to  the  appearance  of  paralysis  of  the  other  side. 
Spasm  of  the  tongue  occasions  difficulties  of  speech.  In  the 
muscles  of  the  neck  it  may  cause  the  position  of  torticollis. 
Spasm  or  contracture  of  the  back  muscles  may  produce  con- 
siderable spinal  curvature.  Contracture  and  swelling  of  the 
abdominal  maiscles  are  the  causes  of  phantom  tumors. 

Tremor  is  an  almost  constant  symptom  of  hysteria  fol- 
lowing accidents.  In  its  most  common  form  it  is  a  fine 
rapid  tremor  of  the  fingers  and  hands,  such  as  occurs  in 
neurasthenia.  It  may  sometimes  imitate  the  tremor  of  pa- 
ralysis agitans  or  the  coarse  inco-ordinated  movements  of 
multiple  sclerosis.  It  becomes  more  marked  under  the  in- 
fluence of  excitement  and  fatigue,  and  usually  disappears 
during  sleep.  In  location  it  may  be  generally  distributed, 
though  it  is  more  commonly  limited  to  certain  groups  of 
muscles. 

There  are  also  a  variety  of  morbid  movements  commonly 
regarded  as  hysterical  in  character,  although  in  many  of 
them  other  hysterical  stigmata  are  absent.  Among  these 
may  be  mentioned  the  rhythmical  chorea  of  Charcot,  para- 
myoclonus multiplex,  and  a  series  of  inco-ordinated  move- 
ments of  forcible  and  shocklike  character. 

In  Charcot's  rhythmical  chorea,  or  chorea  major,  there 
are  alternating  contractions  in  opposing  groups  of  muscles, 
especially  in  those  of  the  hand  and  trunk.  Another  variety 
has  been  called  electrical  chorea,  from  the  sudden  and  forci- 
ble choreiform  muscular  contractions.  It  differs  in  course 
and  in  geographical  distribution  from  the  disorder  named, 
after  its  first  describer,  Dubini's  disease. 

Schutte  has  recently  reported  a  case  of  paramyoclonus 
multiplex  which  seems  to  have  been  one  of  the  ultimate  de- 
velopments of  traumatic  hysteria,  and  which  shows  how 
long  a  time  may  elapse  between  an  accident  and  the  appear- 
ance of  eTxaggerated  symptoms : 


312  FUNCTIONAL   EFFECTS    OF   INJURY. 

The  patient  was  a  man,  fifty-two  years  of  age,  having  no  heredi- 
tary nervous  taint,  who  had  always  been  well  and  strong.  He  fell 
some  little  distance,  striking  his  head.  The  accident  was  followed 
by  weakness,  dizziness,  a  feeling  of  pressure  in  the  head,  and  simi- 
lar subjective  symptoms.  The  patient,  soon  after  the  accident, 
was  pronounced  as  unable  to  work,  and  entitled  to  the  indemnity 
which  the  German  law  allows  in  such  cases.  For  eight  years  he 
presented  the  ordinary  symptoms  of  hystero-neurasthenia.  At  the 
end  of  this  time  he  was  admitted  to  the  hospital,  suffering  from 
the  complication  of  paramyoclonus  multiplex.  The  hysterical 
stigmata,  which  had  been  previously  observed,  had  now  disap- 
peared, and  the  general  condition  was  one  of  neurasthenia,  to 
which  had  been  added  morbid  muscular  movements.  These  move- 
ments were  more  marked  in  the  muscles  of  the  trunk,  and  con- 
sisted of  fibrillary  twitchings  and  forcible  clonic  contractions. 
The  arms  and  legs  were  involved  to  a  less  degree.  On  making 
intended  movements  many  muscles  not  necessary  for  the  move- 
ment were  called  into  play.  During  sleep,  and  when  the  patient 
was  at  rest,  the  clonic  spasms  ceased,  but  the  fibrillary  twitchings 
continued.  The  sleep  was  disturbed.  The  tendon  reflexes  were 
active,  and  there  was  a  slight  bilateral  foot  clonus.  It  was  an  ap- 
parently typical  case  of  paramyoclonus  multiplex,  and  is  one  of  the 
few  recorded  examples  of  that  symptom-complex  resulting  from 
traumatism. 

Hysterical  Joints. — Hysterical  joint  affections  were  rec- 
ognized and  described  by  Brodie,  and  since  his  time  have 
become  familiar  pictures  to  surgeons.  They  are  frequently 
the  sequelae  of  accidents,  after  which  they  may  appear  imme- 
diately, although  there  is  usually  the  intervening  meditative 
period.  Their  development,  when  it  once  begins,  is  usually 
rapid.  In  more  than  one  half  the  cases  the  knee  is  the  joint 
affected  ;  after  it,  in  order  of  frequency,  come  the  hip,  wrist, 
shoulder,  and  ankle. 

The  most  prominent  manifestation  of  hysterical  joint  af- 
fections is  pain  which  is  very  much  intensified  by  any  move- 
ment. Discriminating  examination  shows,  however,  that  the 
hyperalgesia  is  in  the  skin  rather  than  in  the  joint  itself. 
The   hypersensitiveness   is   not   necessarily    limited    to   the 


TRAUMATIC    HYSTERIA.  313 

region  of  the  articulation,  as  in  organic  disease,  but  may  in- 
volve the  whole  limb.  The  position  in  which  the  limb  is 
held  does  not  always  indicate  the  functional  nature  of  the 
trouble. 

The  skin  is  not  reddened,  and  oedema  is  rare. 

The  muscles  around  the  joint  are  usually  the  seat  of  con- 
tracture, with  or  without  paralysis,  and  in  this  situation  also 
there  are  geometrical  areas  of  anaesthesia. 

In  regard  to  diagnosis  I  can  not  do  better  than  repeat  a 
remark  of  Pitres's  relative  to  an  hysterical  coxalgia  :  "  Ab- 
sence of  redness  and  swelling,  little  or  no  spontaneous  pain, 
no  sensitiveness  on  percussing  the  heel,  neither  retraction 
of  the  muscles  nor  morbid  positions,  which  is  the  organic 
lesion  that  could  persist  for  nearly  two  years  with  a  similar 
category  of  negative  symptoms  ?  " 

Hysterical  joints  are  freely  movable  in  ether  or  chloro- 
form narcosis — a  fact,  however,  which  can  rarely  be  demon- 
strated in  medico-legal  cases.  It  is  well  shown  in  a  case  of 
Charcot's  : 

The  patient  was  a  man,  forty-five  years  of  age,  with  negative 
personal  and  ancestral  history.  While  working  at  a  circular  saw, 
the  machine  got  out  of  order,  so  that  he  was  tossed  fifteen  feet  in 
the  air,  coming  down  on  the  buttocks.  There  was  no  loss  of  con- 
sciousness nor  fracture  or  dislocation  of  any  bone.  The  left  foot 
was  slightly  bruised,  but  the  patient  got  up  and  walked  a  short 
distance.  Very  soon,  however,  he  found  that  he  could  not  touch 
the  left  foot  to  the  floor  without  much  pain  in  the  whole  left  leg. 
The  left  leg  soon  became  so  contracted  that  the  knee-jerk  on  that 
side  could  not  be  obtained,  and  movement  at  the  hip  became  very 
limited.  When  the  patient  was  sitting,  the  left  lower  extremity  was 
extended,  not  touching  the  floor.  On  attempting  to  rise,  the  mus- 
cles of  the  arms  were  called  into  play ;  in  order  to  avoid  movement 
of  the  thigh  muscles  when  standing  (Fig.  54),  the  whole  weight  of 
the  body  rested  on  the  right  leg,  causing  the  left  side  of  the  pelvis 
to  be  tilted  up.  There  was  also  considerable  curvature  of  the  spine, 
the  convexity  being  toward  the  right ;  the  left  leg  and  thigh  were 
slightly  carried  forward,  so  that  the  great  toe  of  the  left  side  was 
twenty  centimetres  higher  than  that  of  the  right.     Measurement 


314 


FUNCTIONAL  EFFECTS  OF  INJURY. 


showed  no  real  shortening.  The  movements  at  the  hip  joint  were 
very  limited  and  caused  expressions  of  great  pain.  The  surround- 
ing muscles  were  rigidly  contracted,  and  the  overlying  skin  was 
insensible  to  pricks.     There  were  many  other  hysterical  stigmata. 

The  man  was  put 
under  deep  chloro- 
form narcosis,  when  it 
was  found  that  all 
movement  at  the  hip 
could  be  freely  made. 
When  the  patient  first 
recovered  from  the  ef- 
fects of  the  anaesthetic, 
movements  at  the  hip 
were  painless  ;  but 
when  his  attention 
had  rested  a  short 
time  on  the  affected 
joint  the  old  train  of 
symptoms  returned. 

An  hysterical  joint 
may  remain  useless 
for  w^eeks  or  months. 
When  of  long  dura- 
tion the  condition  is 
liable  to  be  seriously 
complicated  by  or- 
ganic anchylosis,  so  that  the  joint  may  remain  motionless 
through  the  formation  of  adhesions,  long  after  all  the  hys- 
terical symptoms  have  passed  away.  Under  the  influence 
of  emotions,  the  hysterical  joint  affections  may  disappear 
suddenly.     In  such  cases  relapses  are  frequent. 

Reflexes.— Pathological  exaggeration  of  reflex  activity  is 
not  the  rule  in  hysteria,  although  the  tendon  reflexes  are 
often  overactive.  Foot  clonus  is  extremely  rare,  yet  I  have 
seen  foot  clonus  in  a  case  of  paraplegia  which  presented 
every  other  hysterical  symptom,  and  which  eventually  re- 
covered. 


Fig.  54. — Attitude  in  a  case  of  hysterical  coxalgia. 
(After  Richer  and  Berbez.) 


TRAUMATIC    HYSTERIA. 


315 


The  tendon  reflexes  may  be  diminished,  though  never 
lost,  in  a  paralyzed  limb.  This  is  particularly  frequent 
when  anassthesia  is  present  as  well  as  paralysis.  The  plan- 
tar and  conjunctivo-palpebral  reflexes  are  commonly  absent, 
but  the  abdominal  and  cilio-spinal  are  sometimes  retained, 
even  when  there  is  cutaneous  anassthesia. 

Sphincters. — Impairment  of  sphincter  control  in  hysteria 
is  very  unusual.  The  paroxysm  passes  without  involuntary 
micturition,  and  the  various  forms  of  paralysis  are  usually 
unassociated  with  either  rectal  or  vesical  disturbances. 
There  may  be  a  frequent  desire  to  urinate,  due  to  psychic 
rather  than  to  local  conditions,  and  spasm  of  the  neck  of  the 
bladder,  resulting  in  retention  of  urine,  occurs  in  some  cases 
of  paraplegia.  The  mucous  membranes  of  the  bladder  and 
rectum  rarely  if  ever  lose  their  sensibility.  If  they  do,  it  is 
easy  to  understand  how  involuntary  passage  of  urine  or 
fceces  might  occur.  But  the  most  competent  observers  ad- 
mit that  loss  of  sphincter  control  is  among  the  most  unusual 
of  hysterical  accidents. 

The  Hysterical  Attack.  —  The  gra^ide  attaqtie  of  the 
French  consists  of  four  periods:  i,  epileptiform;  2,  period 
of  clownism ;  3,  period  of  passionate  attitudes ;  4,  period 
of  delirium.  Although  it  has  been  observed  in  other 
Continental  countries,  it  is  only  in  France  that  the  grand 
attack  is  often  seen  in  its  full  sequence  of  development. 
Bernheim  calls  it  the  ''  attack  of  culture."  It  seems  proba- 
ble that  the  aggregation  of  so  many  h3^sterical  patients  as 
are  assembled  in  the  Salp^triere  may  have  furnished  sug- 
gesting influences  for  the  induction  of  exaggerated  symp- 
toms. In  this  country  the  hysterical  attack  is  uncommon. 
Knapp  estimates  it  as  occurring  in  ten  per  cent  of  traumatic 
cases.  Even  then  it  never  follows  the  complete  type,  but  is 
manifested  by  the  epileptiform  period  alone,  or  by  emotional 
excitement,  or  by  other  parts  of  the  grand  attack.  The  term 
hystero-epilepsy,  which  has  been  applied  to  the  convulsions 


3i6  FUNCTIONAL   EFFECTS   OF    INJURY. 

of  hysteria,  is  a  misnomer  which  has  led  to  much  confusion. 
The  disease  is  either  hysteria  or  epilepsy,  or  the  two  diseases 
occurring  simultaneously  in  the  same  individual.  Although 
in  many  cases  these  two  diseases  occur  together,  and  al- 
though it  may  be  impossible  to  distinguish  between  them,  it 
is  better  to  state  that  such  is  the  case  than  to  employ  a  mis- 
leading and  indefinite  nomenclature.  There  are  marked  dif- 
ferences between  epileptic  and  hysterical  fits.  In  epilepsy 
the  convulsion  is  of  short  duration,  is  not  necessarily  pre- 
ceded by  an  aura,  and  occurs  very  frequently  at  night.  The 
duration  of  a  hysterical  attack  may  be  a  half  hour  or  more. 
An  aura  is  constant,  and  nocturnal  occurrence  is  exceptional. 
Biting  of  the  tongue  and  involuntary  passage  of  urine,  almost 
constant  phenomena  in  epilepsy,  do  not  occur  in  hysteria. 
During  the  seizure  the  pupil  almost  always  reacts  to  light  in 
hysteria,  not  in  epilepsy,  and  after  the  epileptic  attack  the 
knee-jerk  is  lost,  which  is  not  necessarily  the  case  in  hysteria. 

Furthermore,  the  convulsive  movements  of  hysteria  have 
an  exaggerated  character ;  the  period  of  tonic  contraction  is 
longer  than  in  epilepsy ;  opisthotonos  is  common.  At  the 
expiration  of  the  epileptic  attack  the  patient  commonly  goes- 
into  the  condition  known  as  post-epileptic  stupor ;  from  the 
hysterical  epileptiform  attack  the  patient  usually  recovers 
immediately. 

The  attacks  of  hysteria  may  follow  any  of  the  causes 
capable  of  inducing  other  hysterical  phenomena.  They  are 
sometimes  very  frequent,  occurring  many  times  a  day,  or  at 
certain  hours  of  each  day.  If  they  take  place  once,  they 
will  usually  recur.  After  an  attack  new  symptoms  may  ap- 
pear, or  existing  stigmata  be  made  worse.  Convulsive  hj's- 
teria  is  a  grave  form  of  the  psychosis. 

A  not  uncommon  equivalent  of  the  hysterical  attack  is 
the  so-called  hysterical  coma.  The  cases  I  have  seen  were 
in  men  who  were  brought  to  the  hospital  absolutel}'  uncon- 
scious.     The}^   were    limp,   inanimate   masses,   incapable   of 


TRAUMATIC    HYSTERIA.  ^17 

being  aroused  by  any  stimulation.  The  vascular  and  respi- 
ratory functions  were  normal.  After  a  varying  number  of 
hours  the  patients  would  wake  up  and  walk  home. 

From  the  frequency  with  which  they  are  found  lying 
senseless  in  the  street,  many  of  them  come  to  be  individu- 
ally known  to  ambulance  surgeons,  who,  when  they  pick 
them  up,  recognize  both  the  condition  and  the  individual. 

Hysterical  coma  may  in  many  ways  resemble  apoplexy, 
especially  if  it  be  complicated  by  hysterical  hemiplegia.  The 
functional  character  of  the  affection,  however,  usually  be- 
comes evident  if  all  the  factors  concerned  are  carefully  ex- 
amined. 

In  a  case  of  Comby's  a  nervous  woman,  thirty-eight  years  of 
age,  without  previous  hysterical  accidents,  fell  senseless  as  a  re- 
sult of  a  flash  of  Hghtning  which  killed  two  of  her  children  who 
were  standing  near  her.  The  woman  was  comatose  for  four  days. 
When  consciousness  returned  she  was  hemiplegic  and  hemianaes- 
thetic  on  the  left  side,  a  condition  which  disappeared  entirely  in 
three  weeks.  Two  years  after  this,  during  a  thunderstorm,  the 
patient  again  became  comatose  for  seven  or  eight  hours,  awaken- 
ing to  find  herself  again  hemiplegic  and  hemiansesthetic.  In  two 
weeks  she  was  again  perfectly  well.  Three  years  later  a  similar 
sequence  of  symptoms  was  observed  by  Comby.  The  patient 
was  picked  up  unconscious  in  the  street,  and  brought  to  the  hos- 
pital. The  coma  lasted  four  hours.  Examination  then  showed : 
Facial  expression  good.  No  fever.  Appetite  excellent.  The 
whole  left  side  was  completely  paralyzed.  The  left  arm  lay  immo- 
bile by  the  side  of  the  body  and,  when  lifted  up,  it  fell  lifelessly  to 
the  bed.  The  patient  was  unable  to  raise  the  hand  from  the  bed 
or  to  spread  the  fingers  apart.  There  was  a  slight  paralysis  of 
the  lower  branch  of  the  left  facial  nerve  (this  is  a  rather  uncom- 
mon though  not  an  impossible  symptom  of  hysteria) ;  the  move- 
ments of  the  tongue  and  of  other  muscles  of  deglutition  and  of 
articulation  were  also  impaired.  Knee-jerks  present.  No  foot 
clonus.  All  forms  of  sensibility  of  the  skin  and  mucous  mem- 
branes were  completely  abolished  on  the  left  side.  Vision,  hear- 
ing, smell,  and  taste  were  also  absent  on  the  left. 

In  fifteen  days  all  these  symptoms  disappeared,  and  the  pa- 
tient walked  out  of  the  hospital  apparently  as  well  as  ever. 


3i8  FUNCTIONAL   EFFECTS   OF   INJURY. 

Deaf-mutism  is  a  rare  accident  of  hysteria.  That  it  may 
occur  as  a  result  of  injury  is  shown  by  the  following  case, 
reported  by  Francotte : 

A  man,  thirty-five  years  of  age,  who  had  previously  had  hys- 
terical accidents,  was  bitten  on  the  leg  by  a  dog.  He  was  very 
much  frightened,  and  so  confused  that  he  was  taken  in  charge  by 
the  police.  When  he  arrived  at  the  station  he  had  lost  all  power 
of  speech,  and  was  completely  deaf.  Francotte  saw  the  patient 
nine  days  after  the  accident.  During  that  time  he  had  uttered  no 
sound,  and  could  only  communicate  with  others  by  gestures,  or 
understand  what  was  addressed  to  him  by  writing.  The  case  was 
cured  by  hypnotism. 

Hiccough  and  cough  are  common  symptoms  of  hysteria. 
Blood  is  sometimes  vomited  or  coughed  up  immediately 
after  the  accident.  Anuria  may  occur,  but  the  passage  of 
large  quantities  of  pale  urine  is  more  frequently  observed. 
Ordinarily  the  urine  shows  no  characteristic  chemical 
changes,  although  occasionally  temporary  glycosuria  has 
been  found.     Nutrition  may  be  seriously  affected. 

The  other  symptoms  of  traumatic  hysteria  resemble  those 
described  under  neurasthenia.  There  may  be  a  variety  of 
subjective  symptoms,  of  which,  perhaps,  the  commonest  is 
the  globus  hystericus.  Cardiac  irritability  and  digestive 
disturbances  are  frequently  observed.  There  may  be  con- 
tinued vomiting.  Constipation  is  the  rule.  The  respiration 
is  ordinarily  normal,  but  becomes  very  rapid  through  emo- 
tional influence.  After  nervous  shocks,  or  local  irritation  of 
the  throat,  the  voice  may  be  lost.  Either  aphonia,  in  which 
the  patient  loses  the  power  of  uttering  any  sound,  or  mutism, 
in  which  the  power  of  speech  is  lost,  are  frequent  hysterical 
symptoms.  As  Pitres  has  pointed  out,  hysterical  mutism  is 
often  an  isolated  accident,  which  may  be  observed  in  per- 
sons entirely  free  from  previous  nervous  symptoms  or  active 
hysterical  manifestations. 

Prognosis. — That  death  may  occur  as  a  result  of  hysteria 
uncomplicated  by  organic  disease,  appears  to  be  a  matter 


TRAUMATIC    HYSTERIA.  3  in 

of  considerable  doubt,  although  such  a  possibility  is  ad- 
mitted by  most  authorities.  Gilles  de  la  Tourette  quotes 
several  cases  in  which  hysteria  is  said  to  have  been  the  cause 
of  death.  The  immediate  causes  in  the  cases  least  open  to 
criticism  were  due  to  spasm  of  the  throat  and  of  the  stom- 
ach, and  from  exhaustion  induced  by  long  vomiting, 

A  patient  at  St.  Luke's  Hospital  several  years  ago  presented 
the  hysterical  symptoms  of  hemiansesthesia,  contraction  of  the 
visual  fields,  and  epileptiform  convulsions,  but  we  could  discover 
no  evidences  of  any  organic  disease.  The  man  was  found  one 
morning  dead  in  bed.  The  autopsy  revealed  no  causes  such  as 
are  usually  regarded  as  adequate  to  induce  death. 

There  are,  however,  so  far  as  I  know,  no  cases  of  hysteria 
reported  as  fatal  in  which  microscopical  examination  had 
excluded  visible  pathological  alterations  of  nervous  tissue. 
That  careful  and  thorough  examination  in  accordance  with 
modern  microscopical  methods  is  necessary  before  it  can  be 
said  that  a  nervous  disease  is  functional,  has  been  thoroughly 
demonstrated  by  the  history  of  Landry's  paralysis,  a  disor- 
der which  formerly  was  thought  to  be  characterized  by  no 
discoverable  lesions,  but  which  has  recently  been  shown  to 
be  due  to  degeneration  of  the  ganglion  cells  in  the  spinal 
cord  and  in  the  brain. 

As  we  have  seen,  many  cases  of  traumatic  hysteria  are 
somewhat  different  from  hysteria  when  it  occurs  from 
causes  other  than  traumatisms.  In  traumatic  cases,  impair- 
ment of  general  nutrition  may  render  the  patient  less  ca- 
pable of  resisting  the  ordinary  injurious  influences  of  daily 
life.  Nevertheless,  even  in  them,  the  prognosis  of  hysteria  in 
regard  to  life  is  very  good.  As  regards  complete  recovery, 
it  is  much  less  favorable  than  that  of  traumatic  neuras- 
thenia. 

The  patient  with  traumatic  hysteria  may  be  relieved  of 
his  paralyses  or  contractures  more  speedily  than  the  neuras- 
thenic is  rid  of  his  lumbago.     Yet  the  disease  often  remains. 


320  FUNCTIONAL   EFFECTS   OF    INJURY. 

ready  to  show  itself  again  under  the  influence  of  suggestion 
or  emotion,  although  its  paroxysmal  symptoms  have  disap- 
peared. Although  some  cases  get  entirely  well  in  a  few 
weeks  or  months,  never  to  relapse,  there  is  a  general  agree- 
ment of  authority  that  the  disordered  mental  state  of  hys- 
teria, which  is  the  cause  of  the  symptoms,  is  an  extremely 
tenacious  condition,  and  that  the  prognosis  in  any  given 
case  is  always  attended  with  uncertainty. 

There  are  some  considerations,  however,  which  to  a  cer- 
tain extent  are  of  value  in  reaching  a  prognosis.  Among 
the  most  important  of  these  is  predisposition,  which  has  oc- 
curred through  enfeeblement  of  the  resisting  powers  of  the 
nervous  system  by  transmitted  ancestral  defects  or  by  ac- 
quired exhaustion.  Such  predisposition  is  only  occasionally 
discoverable  in  traumatic  hysteria,  and  the  chances  for  re- 
covery are  naturally  best,  as  in  certain  forms  of  insanity,  in 
the  patients  whose  personal  and  ancestral  record  is  free  from 
nervous  stigmata.  As  regards  age,  it  may  be  said  that  the 
younger  the  patient  the  better  are  the  hopes  for  ultimate 
recovery.  It  must  not  be  forgotten,  however,  that  when 
hysteria  appears  in  children  there  may  often  be  found  a 
strong  hereditary  predisposition  to  nervous  disease.  This 
fact  mav  more  than  counterbalance  the  favorableness  of  the 
prognosis  caused  by  youth.  Hysteria  in  men  is  attended 
with  a  more  serious  prognosis  than  in  women. 

The  prognosis  is  better  for  the  well-to-do  classes,  for  in 
them  proper  treatment  can  usually  be  instituted.  The  treat- 
ment, which  is  a  regulation  of  the  mode  of  life  rather  than  a 
treatment  by  drugs,  is  expensive,  and  can  only  occasionally 
be  properly  carried  out  in  the  working  classes. 

In  regard  to  litigation,  what  is  true  for  the  prognosis  of 
traumatic  neurasthenia  may  be  made  still  more  emphatic  for 
traumatic  hysteria.  The  constant  questionings  and  exami- 
nations by  lawyers  and  doctors  are  most  potent  suggesting 
influences.     They  render  the  consciousness  still  more  lim- 


TRAUMATIC    HYSTERIA.  32 1 

ited,  and  give  an  increased  permanency  to  the  fixed  ideas  of 
the  hysterical  patient. 

Repeated  examinations  of  a  limb  which  is  the  seat  of 
hysterical  paralysis  render  the  toss  of  power  more  pro- 
found and  more  permanent:  repeated  tests  for  sensation 
cause  anaesthesia  to  deepen,  to  spread,  or  to  appear  in  new 
places ;  it  is  well  known  that  the  symptoms  of  hysteria  often 
owe  their  genesis  to  the  suggesting  influences  of  hospital 
life ;  all  these  agencies  are  most  prejudicial  to  ultimate  re- 
covery. It  is  the  evil  results  which  attend  suggestion  of 
any  kind  upon  the  hysterical  mind  that  has  led  to  the  gen- 
eral abandonment  of  the  use  of  hypnotism— a  procedure 
which  may  cause  a  symptom  to  temporarily  disappear,  but 
which  involves  the  danger  of  aggravating  the  mental  state. 

The  hysterical  patient  is  very  suggestible  even  when  not 
hypnotized,  and  constant  examinations  almost  invariably 
suggest  to  him  that  the  symptoms  remain  stationary  or  be- 
come worse. 

Recovery  from  hysteria  is  possible,  even  when  the  dis- 
order has  occurred  in  an  aggravated  form.  But,  as  a  rule, 
the  more  numerous  and  severe  the  symptoms,  the  less  it  is 
probable  that  the  patient  will  ever  be  free  from  the  disease. 

The  exaggerated  psychical  phenomena  are  of  especially 
serious  import,  as  they  denote  a  profound  disturbance  of 
mental  function.  The  attacks,  catalepsy,  trance,  and  coma, 
indicate  that  the  disease  is  severe,  and  that  it  has  probably 
developed  in  a  predisposed  brain. 

Some  of  the  stigmata,  such  as  the  anaesthesias  and  visual 
disturbances,  are  particularly  tenacious. 

Recovery  from  the  joint  affections  is  usually  slow.  They 
may  frequently  relapse  or  last  for  several  years,  and  may 
eventually  cause  permanent  organic  disabilities. 

There  are  no  means  of  foretelling  how  long  a  hysterical 
paralysis  may  last. 

In  a  case  of  Page's,  paraplegia  existed  for  four  years  and 


322  FUNCTIONAL   EFFECTS   OF   INJURY. 

a  half,  and  in  a  patient  of  mine,  whom  I  have  mentioned,  the 
left  leg  has  been  paralyzed  for  two  years.  Zein  reports  a 
case  of  hysterical  paraplegia  in  which  recovery  took  place 
after  nineteen  years  ;  and  Morton  Prince  has  seen  three  cases 
of  hysterical  paralysis  (two  monoplegias  and  one  hemiplegia 
and  hemiansesthesia)  which  began  in  the  War  of  the  Rebel- 
lion and  which  had  existed,  one  for  twenty-eight  and  two 
for  twenty-nine  years. 

The  brachial  monoplegias  seem,  as  a  rule,  the  least  per- 
sistent of  the  individual  forms  of  paralysis. 

The  prognosis  of  mutism,  or  aphonia,  is  nearly  always 
good  ;  speech  is  usually  restored  in  a  few  weeks  or  months. 
But  all  of  these  symptoms  are  liable  to  relapse,  and  it  is 
never  justifiable  to  consider  the  hysteria  as  cured  because 
all  the  paroxysmal  symptoms  disappear. 

The  relapses,  which  may  be  more,  or  less  severe  than  the 
conditions  which  preceded  them,  follow  very  shortly  after 
apparent  cure,  or  are  separated  by  considerable  periods  of 
time. 

The  rapidity  with  which  hysterical  symptoms  may  van- 
ish, and  become  re-established,  is  well  shown  by  a  case  seen 
with  Dr.  G.  E.  Brewer  at  the  City  Hospital : 

A  man,  thirty-eight  years  of  age,  alcohoHc,  fell  in  the  street 
and  found  both  legs  paralyzed.  When  brought  to  the  hospital  he 
presented  the  classical  symptoms  of  hysterical  paraplegia — viz., 
great  rigidity  of  the  legs,  inability  to  walk,  and  anaesthesia,  with 
perfect  control  of  the  bowels  and  bladder.  He  was  put  on  appro- 
priate treatment,  and  recovered  so  completely  that  in  a  few  days 
he  walked  out  of  the  hospital  in  a  perfectly  normal  way.  About 
ten  days  later  I  was  asked  by  Dr.  Frank  Markoe  to  see  a  case  in 
his  wards  at  Bellevue  Hospital.  It  was  of  a  man  who  had  been 
found  lying  in  the  street  with  both  legs  paralyzed.  The  patient 
was  the  same  man  that  had  been  seen  at  the  City  Hospital. 

Bibliography. 

(The  reader  is  especially  referred  to  the  comprehensive  treatise 
of  M.  de  la  Tourette.) 


TRAUMATIC    HYSTERIA.  323 

Babinski,  Contractures  organiques   et   hysteriques.      Soc.  niH. 

^^^ /2^/.,  Mai,  1893.  ,.    ,^   ,     „         7  -r^ 

Bailey  A  Case  of  General  Analgesia.  N.  Y.  Med.  Record,  De- 
cember 28,  1895.  Ibid.,  The  Diagnosis  of  Idiopathic  Epilepsy. 
Am.  Med.  Surg.  Bui.,  August  8,  1896. 

Berbez,  Hysteric  et  traumatisme.     These  de  Pans,  1887. 

Bernhe'im,  Hypnotisme,  Suggestion,  Psychotherapie,  1891. 

Bremer,  A  Case  of  Hysterical  Astasia-abasia  suing  for  Dam- 
ages.    Journ.  Nerv.  a7id  Ment.  Dis.,  1893,  p.  13. 

Briquet,  Traite  clinique  et  therapeutique  de  I'hysterie,  1859. 

Blocq  Sur  une  affection  caracterisee  par  de  I'astasie-abasie. 
Arch,  de  neural.,  1888.  Ibid.,  Les  troubles  de  la  marche  dans  les 
maladies  nerveuses.     Paris.  ■      .  rr 

Brodie,  Lectures  Illustrative  of  Certain  Local  Nervous  Affec- 
tions.    London,  1837. 

Charcot,  CEuvres  completes.     Paris,  1890. 

Comby  J  ,  Apoplexie  hysterique  avec  hemiplegie  gauche  sur- 
venue  pour  la  premiere  fois  a  la  suite  d'une  fulguration.      Union 

med.,  1894,  No.  60. 

Dana,  C.  L.,  Hamilton's  System  of  legal  Medicine,  New  York, 


'   ^Francotte,  Sourd-muettite   hysterique,  etc.     Mercredi  m'edical, 

1894,  No.  40. 

Guinon,  Les  agents  provocateur  de  I'hysterie.     Pans,  1889. 
Hun,  Two  Cases  of  Traumatic  Hysteria.     Medical  News,  April 

II,  1891,  p.  403-  ,     ^     . 

Janet,  Etat  mental  des  hysteriques.     2  vols.  Fans. 

Knap'p,  Traumatic  Hysteria.  Text-book  of  Nervous  Diseases  by 
American  Authors,  Philadelphia,  1895.. 

Konig,  Weitere  Mittheilungen  iiber  die  functionellen  Gesichts- 
feldanomilien  mit  besonderer  Berucksichtigung  von  Eefunden  an 
normalen  Menschen.    Deutsch.  Zeits.f  Nervenh.,  1895,  vol.  vii,  p.  263. 

Laehr,  Ueber  Storungen  der  Schmerz  und  Temperaturempfin- 
dung  in  Folge  von  Erkrankungen  des  Ruckenmarkes.     Arch,  fiir 

Psych.,  1896,  3,  p.  773-  ,     „  ^ 

Laudan,  Ein    Fall   von  Catalepsie.      Wien.   med.   Presse,    1894. 

Nos.  30  and  35.  ■  a     1, 

Lebrun,    Monoplegie    brachiale    hystero-traumatique.     Arch. 

med.  Beiges,  1893,  vol.  i,  p.  382. 

Lepois,  quoted  by  Gilles  de  la  Tourette,  op.  cit.,  1,  p.  13- 
Miura,  Trois  cas  de  monopl6gie  brachiale  hysterique.     Arch, 

de  Neurol.,  Mai,  1893. 


324  FUNCTIONAL   EFFECTS   OF   INJURY. 

Mobius,  Ueber  den  Begriff  der  Hysteric.  Neurolog.  Beitrdge,  i, 
1894. 

Page,  H.  W.,  Injuries  of  the  Spine  and  Spinal  Cord,  witliout 
Apparent  Mechanical  Lesion  and  Nervous  Shock  in  their  Surgical 
and  Medico-legal  Aspects.  London,  1883.  Ibid.,  Railway  Injuries 
in  their  Clinical  and  Medico-legal  Aspects.     London,  1891. 

Paget,  Clinical  Lectures  and  Essays.  Second  edition,  Lon- 
don, 1879. 

Peterson,  Physiological  Experiments  with  Magnetism  at  the 
Edison  Laboratory.     JV.  Y.  Med.  Jour.,  December  31,  1892. 

Pitres,  Lepons  cliniques  sur  I'hysterie  et  I'hypnotisme.  Paris, 
1891. 

Prince,  Three  Cases  of  Traumatic  Hysterical  Paralysis  of 
Twenty-nine,  Twenty-eight,  and  Twenty-nine  Years'  Duration 
respectively  in  Males.     A771.  Jour,  of  the  Med.  Sci.,  1892,  p.  63. 

Ibid.,  Hysterical  Monocular  Amblyopia.  Am.  Jour,  of  the  Med. 
Sci.,  February,  1897. 

Richer,  Etudes  cliniques  sur  la  grande  hysteric,  etc.    Paris,  1885. 

Reynolds,  Russell,  Paral)^sis  and  other  Disorders  of  Motion 
and  Sensation  dependent  on  Idea.  Brit.  Med.  Journal,  1869, 
vol.  ii,  p.  483. 

Schutte,  E.,  Ein  Fall  von  Paramyoclonus  Multiplex  bei  einem 
Unfallskranken.     Neurolog.  Cblatt.,  1897,  No.  i. 

Serieux,  Note  sur  un  cas  de  paralysie  hystero-traumatique  des 
quatre  membres.     Arch,  de  Neurologie,  July,  1891,  p.  31. 

Souques,  Etude  des  syndromes  hysteriques  "  simulateurs." 
Paris,  189 1. 

Striimpell,  Ueber  die  traumatische  Neurosen.  Berlin.  Klin., 
1888,  Heft  3. 

Sydenham,  quoted  by  Gilles  de  la  Tourette,  op.  cit.,  i,  p.  15. 

Tourette,  de  la,  Gilles,  Traite  clinique  et  therapeutique  de 
I'hysterie.     3  vols,  Paris,  1891  and  1895. 

Zein,  quoted  by  Gilles  de  la  Tourette,  op.  cit.,  vol.  ii,  p.  no. 


CHAPTER   IV. 

UNCLASSIFIED    FORMS. 

In  the  preceding  pages  it  has  been  repeatedly  empha- 
sized that  the  diagnosis  of  the  traumatic  neuroses  depends 
upon  the  possibility  of  a  clinical  separation  between  organic 
and  functional  nervous  diseases.  When  an  organic  lesion  is 
caused  by  injury,  certain  definite  signs,  which  are  ordinarily 
absent  in  functional  disorders  and  which  point  to  injury  in 
definite  areas  of  nervous  tissue,  usually  present  themselves 
at  once.  Yet,  while  it  is  generally  possible  to  draw  the 
dividing  line  with  reasonable  exactness,  and  to  infer  from  the 
circumstances  of  the  accident  and  from  the  character  of  the 
symptoms  the  probable  nature  of  the  pathological  process, 
there  remains  a  group  of  cases  which  can  not  be  satisfac- 
torily classified.  Although  they  present  many  of  the  symp- 
toms of  hysteria  and  neurasthenia,  their  clinical  course  is 
more  serious  than  is  customarily  observed  in  these  disorders, 
and  some  symptoms  are  present  which,  while  not  giving 
positive  evidences  of  definite  focal  injury,  are  different 
from  those  usually  brought  about  by  the  impaired  mentality 
of  hysteria  or  the  over-fatigue  of  neurasthenia.  These  are 
transition  types,  and  bear  testimony  to  the  artificial  charac- 
ter of  the  distinction  between  "organic"  and  "functional" 
-disease.  They  have  received  various  names,  and  have  been 
the  object  of  much  pathological  speculation.  By  Dana  they 
are  called  the  "grave  traumatic  neurosis,"  on  account  of 
their  unfavorable  prognosis.  Crocq  denominates  them  as 
■"  the    grave  traumatic  neurosis,  with   probable  organic  le- 

22  325 


326  FUNCTIONAL   EFFECTS   OF    INJURY. 

sions."  Knapp,  reasoning  from  the  analogy  of  the  organic 
character  of  some  of  the  symptoms,  from  certain  correlated 
experiments  on  animals  and  from  the  results  of  a  few  hu- 
man autopsies,  goes  still  further,  and  gives  to  them  the 
name  of  "  traumatic  sclerosis." 

As  clinical  occurrences  they  are,  in  my  experience,  dis- 
tinctly rare.  Of  the  large  number  of  patients  with  nervous 
diseases  coming  to  the  Vanderbilt  Clinic  in  the  past  few 
years,  none  are  recorded  as  belonging  to  this  class.  Dana 
also  considers  them  infrequent.  Knapp,  on  the  other  hand, 
has  met  with  them  more  often.  Some,  but  not  all,  of  the 
cases  recorded  by  Oppenheim  in  his  Traumatic  Neuroses 
may  properly  be  classed  with  these  unusual  forms.  Rela^ 
tive  to  frequency  it  may  be  remarked  that  his  cases,  al- 
though they  were  collected  during  a  period  of  eight  years 
from  the  large  nerve  clinic  of  the  Charity,  in  Berlin,  were 
only  forty-two  in  number.  It  is  partly  owing  to  Oppen- 
heim's  description  that  so  much  confusion  has  arisen  con- 
cerning the  nature  of  the  conditions  which  most  frequently 
result  from  injury  and  shock.  Many  persons  have  inferred 
that  the  symptomatology,  as  detailed  by  the  German  neu- 
rologist, was  intended  to  apply  to  all  the  affections  em- 
braced in  the  term  traumatic  neuroses.  Such  an  interpre- 
tation, however,  was  not  Oppenheim's  intention.  Although 
cases  similar  to  some  of  those  which  he  describes  are  in- 
frequent, that  they  occasionally  occur  there  can  be  no  doubt. 
My  own  experience  with  them  has  been  slight,  and  in  de- 
scribing them  I  shall  be  obliged  to  rely  chiefiy  upon  facts 
as  reported  by  other  observers. 

iEtiology. — The  accident  which  gives  rise  to  these  cases 
has  usually  been  severe.  Considerable  injury  of  the  body  is 
the  rule.  Psychic  shock  is  sometimes,  but  not  always, 
present.  In  a  case  of  Knapp's,  which  ended  fatally,  "  a 
woman  was  dragged  in  a  railw^ay  collision,  her  head  and 
back  bumping  over  the  slee|)ers."     Such  accidents  as  are  of 


UNCLASSIFIED   FORMS.  327 

not  uncommon  occurrence  in  factories,  in  which  the  body 
may  be  seriously  lacerated  by  revolving  machinery,  or  tossed 
about  by  explosions,  are  most  frequently  followed  by  the 
■serious  forms.  Falls  on  the  head  from  great  heights,  or  any 
accidents  in  which  the  victims  are  subjected  to  very  severe 
concussions,  contusions,  and  wounds  constitute  their  most 
frequent  starting  points.  From  the  comparative  immunity 
from  exposure  to  such  injuries  among  the  well-to-do  classes, 
the  grave  traumatic  neuroses  are  most  commonly  observed 
in  laborers  and  factory  hands,  or  in  persons  whose  occupa- 
tions constantly  expose  them  to  danger.  For  similar  rea- 
sons these  disorders  are  most  frequent  in  men. 

Symptoms. — The  onset  of  the  symptoms  is  in  many  respects 
sirhilar  to  the  onset  of  simple  traumatic  hysteria  and  neuras- 
thenia. On  account  of  the  severe  injuries  to  the  body,  there 
is  an  increased  frequency  in  the  occurrence  of  physical  shock, 
and  the  patients  often  remain  unconscious  for  a  considerable 
length  of  time  after  the  accident.  If  there  has  been  exten- 
sive laceration  of  the  body,  the  character  of  the  nervous 
symptoms  may  not  show  itself  until  some  time  after  the 
wounds  have  begun  to  heal.  It  then  becomes  evident  that  it 
is  more  serious  than  is  ordinarily  met  with  in  accident  cases 
in  which  acute  organic  injuries  to  the  nervous  system  are  ab- 
sent. Of  the  mental  symptoms,  depression  is  often  present 
in  a  marked  degree.  The  patient  sits  immobile  and  inatten- 
tive, with  many  of  the  evidences  of  profound  depression. 
He  apparently  takes  no  interest  in  his  condition,  his  pros- 
pects, or  his  family.  If  spoken  to,  he  replies,  but  his  replies 
are  monosyllabic  or  brief.  He  rarely  presents  the  mutism 
of  severe  melancholia,  yet  he  is  impatient  of  all  interference, 
and  wishes  to  be  left  quietly  alone.  He  may  be  seen  crying 
quietly  by  himself.  Suicide  has  occasionally  occurred.  In 
some  cases  the  picture  resembles  dementia  rather  than 
melancholia.  The  patient  becomes  apathetic  and  childish, 
with     considerable    impairment    of     intellectual     capacity, 


528  FUNCTIONAL   EFFECTS   OF   INJURY, 

caused  by  loss  of  memory  and  lack  of  attention.  The  am- 
nesia is  chiefly  for  recent  events,  although  it  may  be  so  pro- 
nounced that  it  is  impossible  for  the  patient  to  distinctly  re- 
call happenings  of  previous  years.  He  forgets  names  and 
words,  but  usually  remembers  faces.  All  details  of  the  acci- 
dent may  be  entirely  forgotten,  especially  if  the  head  injury 
has  been  severe.  The  lack  of  attention  does  not  appear  to 
be  a  lack  of  attention  to  outside  matters  such  as  is  com- 
monly seen  in  introspective  mental  states.  The  patient  ap- 
pears to  be  thinking  not  so  much  about  himself  as  of  noth- 
ing at  all.  It  is  an  inhibition  of  psychic  processes  rather 
than  a  diversion  of  thought  into  morbid  channels.  The 
mental  state  resembles  that  of  hysteria  more  closely  than 
it  does  that  of  neurasthenia,  so  that,  the  patient  is  not  the 
querulous,  petulant  invalid,  but  presents  rather  the  type  of 
the  apathetic  man,  prematurely  old,  who  is  suffering  from  a 
serious  disorder  affecting  the  mind  which  is  characterized 
by  a  limitation  of  all  intellectual  processes. 

Such  a  mental  state  renders  the  patient  incapable  of  pro- 
longed mental  effort.  He  is  entirely  unable  to  work,  and 
often  can  not  keep  his  attention  sufficiently  concentrated  for 
the  performance  of  the  simplest  tasks. 

The  psychic  condition  is  often  revealed  by  the  facial  ex- 
pression. The  face  is  pale,  often  of  a  gra3'ish  appearance, 
and  the  lines  in  the  face  may  be  drawn.  The  expression  is 
indicative  of  absent-mindedness  or  of  depression. 

Disturbances  of  motion  are  the  most  frequent  and  the 
most  pronounced  of  the  physical  symptoms. 

Tremor  is  constant,  and  appears  in  various  ways.  It  is 
usually  a  tremor  which  disappears  when  the  muscles  are  at 
rest,  but  is  very  much  intensified  during  the  execution  of 
intended  movements  and  under  the  influence  of  excitement 
or  fatigue.  It  may  be  nothing  more  than  an  exaggeration 
of  the  common  neurasthenic  tremor,  in  which  form  it  is 
most  commonly  observed  in  the  hands.     The  patient  finds 


UNCLASSIFIED    FORMS. 


329 


it  difficult  to  perform  the  finer  co-ordinated  movements ; 
the  hands  may  tremble  so  much  that  it  is  only  with  diffi- 
culty that  he  can  button  his  clothes.  Similarly,  the  hand- 
writing- is  often  illegible  from  the  uncertainty  and  irregu- 
larity of  the  pen  strokes.  In  other  cases  the  tremor  of  the 
hands  and  arms  is  so  coarse,  and  the  excursions  are  so  ex- 
tensive, exaggerated,  and  jerky,  and  so  much  increased  by 
intended  movements,  that  it  is  very  similar  to  the  tremor 
which  is  seen  in  multiple  sclerosis.  If  the  patient  attempts 
to  touch  the  tip  of  the  nose  with  his  index  finger  when  his 
eyes  are  closed,  he  comes  very  wide  of  the  mark.  Tremor  of 
this  character  renders  the  individual  seriously  incapacitated. 
The  movements  are  so  uncertain  that  the  ordinary  affairs  of 
daily  life  can  only  be  performed  after  deliberation  and  with 
care.  There  may  be  considerable  difficulty  in  eating ;  in 
attempts  to  raise  a  glass  full  of  water  to  the  lips,  the  water 
may  be  spilled  on  the  floor  or  on  the  patient.  The  tremor 
is  usually  most  marked  in  the  hands  and  arms,  although 
sometimes  there  is  shaking  of  the  head  as  well. 

Nonne  has  recently  reported  a  number  of  cases  which 
presented  peculiar  and  characteristic  tremor,  and  in  which 
the  movements  did  not  affect  single  muscles  or  segments  of 
limbs,  but  one  or  both  extremities.  It  was  a  shaking  tremor 
which,  when  sufficiently  intense,  agitated  the  whole  body, 
so  that  the  patient  was  unable  to  either  walk  or  stand.  The 
muscles  of  the  affected  extremities  had  a  marked  tendency 
to  contract,  so  that  they  stood  out  hard  and  tumorlike.  This 
tremor  was  therefore  distinguishable  from  that  of  multiple 
sclerosis,  of  exophthalmic  goitre,  of  paralysis  agitans,  or 
from  that  due  to  hysterical,  senile,  toxic,  or  other  causes. 
In  slight  cases  the  morbid  movements  ceased  during  rest. 
In  severe  cases  they  continued  as  long  as  the  patient  thought 
himself  observed  or  was  excited  in  any  way.  The  gait  of 
these  patients  was  characteristic  from  their  attempts  to 
overcome  the  contractions  of  the  flexor  and  extensor  mus- 


330  FUNCTIONAL   EFFECTS   OF   INJURY. 

cles  of  the  legs,  while  these  extremities,  or  even  the  trunk, 
were  being-  violently  shaken  by  the  tremor.  Cases  similar 
to  those  described  by  Nonne  are  frequently  regarded  as 
simulators.  A  man  presenting  these  motor  symptoms,  who 
was  for  a  time  under  my  observation  at  the  Workhouse,  was 
considered  by  the  guards  to  be  malingering  in  order  to 
escape  being  made  to  work.  In  all  of  Nonne's  cases  the 
symptoms  remained  unchanged  for  several  years,  and  the 
question  of  simulation,  or  even  exaggeration,  could  be  ex- 
cluded. In  one  the  patient  committed  suicide,  after  the 
symptoms  had  existed  for  six  years  : 

Male,  fifty-five  years  of  age.  Ancestral  and  personal  history 
negative.  A  previously  healthy  man.  After  a  fall  on  the  back 
and  head,  by  which  two  ribs  were  broken,  the  patient  found  him- 
self unable  to  walk.  There  was  no  trouble  with  the  sphincters. 
In  six  weeks  after  the  accident  he  could  walk  a  little,  but  never 
was  able  to  return  to  work. 

The  patient  was  examined  one  year  after  the  accident.  He  then 
walked  with  legs  apart  and  knees  slightly  flexed.  There  was  con- 
siderable dorsal  flexion  of  foot  in  walking,  and  he  pushed  himself 
forward  from  the  hips  at  the  same  time,  thereby  showing  vacillation 
and  coarse,  shaking  tremor  in  the  trunk  and  all  extremities.  On 
standing,  a  slight  tremor  of  the  trunk  persisted.  No  Romberg 
symptom.  On  walking,  many  muscles  became  the  seat  of  invol- 
untary contractions,  which  the  patient  could  not  voluntarily  over- 
come. There  was  slight  bilateral  foot  clonus.  All  the  reflexes 
were  active.  The  strength  was  diminished  in  the  upper  extremities 
and  still  more  so  in  the  lower  extremities.  There  was  some  diminu- 
tion of  sensibility  in  the  legs.  There  was  slight  lateral  nystagmus 
and  a  moderate  limitation  of  the  visual  fields.  Speech  was  not  in- 
terfered with.  The  intelligence  was  good,  and  there  was  no  mental 
depression.  Sleep  and  appetite  normal.  The  clinical  picture,  with 
the  exception  of  some  variations  in  cutaneous  sensibility,  remained 
unchanged  for  six  years.  [However,  since  at  the  end  of  this  period 
the  patient  took  his  own  life,  it  is  probable  that  depression  had 
displaced  the  previous  normal  mental  condition.] 

Although  the  gait  in  the  unclassified  forms  does  not  pre- 
sent the  stiff,  dragging,  spastic  character  of  the  gait  of  mul- 


UNCLASSIFIED   FORMS. 


331 


tiple  sclerosis,  it  is  rarely  the  gait  of  a  normal  person.  The 
patients  walk  slowly  and  hesitatingly,  and  may  drag  their 
feet  a  little,  but  the  gait  has  no  evidences  of  true  paralysis  or  of 
contracture.  There  may  be  considerable  swaying  of  the  body 
on  standing  with  closed  eyes.  In  some  cases  there  are  fibril- 
lary twitchings  in  the  muscles,  a  symptom  which  is  especially 
frequent  in  the  muscles  of  the  shoulders  or  of  the  face.  The 
tongue  is  tremulous  as  a  rule,  and  disturbances  of  speech  are 
common.  The  voice  is  thick  and  the  enunciation  indistinct. 
The  speech  defects  differ  from  those  of  simple  traumatic  neu- 
rasthenia in  that  they  are  more  or  less  beyond  the  patient's  con- 
trol. With  the  best  endeavors  and  closest  attention  he  may 
be  unable  to  articulate  clearly.  The  voice  also  often  has  a  jerky 
character,  another  symptom  common  in  multiple  sclerosis. 

Paralysis  can  not  be  recognized  as  a  symptom  of  these 
transitional  forms.  When  there  occurs  a  localized  paralysis, 
it  must  be  explained  as  a  hysterical  symptom  or  as  an  un- 
equivocal indication  of  organic  disease. 

Indeed,  the  characteristic  which  renders  the  classification 
of  these  cases  so  difficult  is,  that  they  present  no  evidences 
which  permit  of  the  diagnosis  of  a  focal  lesion  such  as  may 
be  made  in  cases  of  organic  injury  to  the  nervous  system, 
and  that  the  symptoms  differ  in  character  and  in  association 
from  those  of  the  functional  disorders.  Some  of  the  clinical 
manifestations  of  hysteria,  such  as  ansesthesia  and  contrac- 
tion of  the  visual  field,  may  be  found,  but  paralysis  is  absent. 
Paralysis  may  occur  in  certain  forms  of  hysteria  which  have 
other  severe  symptoms,  but  in  such  cases  the  whole  symptom- 
complex  would  be  usually  explained  by  the  assumption  of 
hysteria  or  hystero-neurasthenia. 

Although  no  muscle  or  muscle  groups  are  paralyzed  in 
the  unclassified  forms,  there  is  a  weakness  in  all  the  muscles. 
The  patients  are  loath  to  make  voluntary  movements,  they 
become  tired  quickly,  and  muscular  exercise  and  fatigue 
cause  an  increase  in  the  other  symptoms. 


332  FUNCTIONAL   EFFECTS   OF    INJURY. 

As  there  is  no  paralysis,  so  there  is  an  absence  of  muscu- 
lar atrophy.  The  whole  muscular  system  may  share  in  the 
general  malnutrition,  but  there  is  no  selective  wasting  of 
muscles.  The  electrical  reactions  usually  remain  normal^ 
although  diminished  excitability  of  the  muscles  to  electricity 
has  been  observed. 

The  deep  reflexes  as  a  rule  are  exaggerated.  The  knee- 
jerks  are  usually  so  active  that  taps  on  or  above  the  knee 
induce  very  quick  and  forcible  muscular  contractions.  In 
some  cases  a  slight  foot  clonus  has  been  observed,  but  this 
symptom  is  rare.  A  few  cases  have  been  described  in 
which  the  knee-jerks  are  diminished,  but  in  no  case  have 
the  knee-jerks  been  said  to  be  lost  when  Jendrassik's  method 
of  re-enforcement  has  been  used.  The  superficial  refiexes 
usually  present  nothing  characteristic,  though  they  some- 
times give  sluggish  or  imperfect  responses  to  stimulation. 
The  abnormal  changes  in  reflex  activity  affect  the  two  sides 
of  the  body  equally. 

Sensory  symptoms  may  be  similar  to  those  observed  in 
simple  traumatic  neurasthenia  or  hysteria,  but  they  are 
much  less  prominent.  If  traumatic  lumbago  is  present  it 
presents  the  ordinary  sympt6"ms  characteristic  of  that  con- 
dition ;  apart  from  lumbago,  pain  in  these  forms  is  not  very 
frequently  or  very  emphatically  complained  of. 

Headache  is  usually  present  in  shght  degrees,  but  it  or- 
dinarily lacks  the  exaggerated  character  of  neurasthenic 
headache.  The  patient  feels  a  tightness  or  constriction 
around  the  head,  the  existence  of  which  he  admits  when 
questioned,  but  of  which  he  only  rarely  complains.  There 
is  usually  some  pain  in  the  back,  and  pressure  over  painful 
areas  may  be  poorly  borne  ;  but  a  characteristic  of  the  pain 
in  these  forms  is  that  it  is  passive  rather  than  active.  There 
are  rarely  heard  the  constant  complaints  (so  common  in 
neurasthenia)  of  terrible  pain  and  hyperaesthesia  which  are 
made  worse  by  every  movement  and  by  every  jar.     If  the 


UNCLASSIFIED   FORMS. 


333 


patient  is  asked  if  he  has  pain  in  certain  parts,  he  may  reply- 
in  the  affirmative,  but  the  complainings  of  constant  pain  and 
exaggerations  of  sensibility  are  usually  absent. 

Anesthesia,  which  has  frequently  been  observed,  differs 
in  important  particulars  from  the  anaesthesia  of  typical  hys- 
teria. In  extent,  distribution,  and  selection  it  resembles  the 
loss  of  cutaneous  sensibility  such  as  is  found  in  the  depress- 
ive and  demented  forms  of  insanity,  more  closely  than  the 
typical  loss  of  sensibility  commonly  occurring  in  hysteria. 
The  sensory  abnormities  are  in  accord  with  the  mental  state 
of  inattention,  indifference,  or  depression,  and  most  fre- 
quently exist  as  a  general  blunting  of  cutaneous  sensibility. 
Slight  touches  on  any  part  of  the  cutaneous  surface  are  im- 
perfectly perceived,  and  pricks  with  sharp  instruments  cause 
only  slight  pain. 

Less  frequently  the  touch  sense  may  be  fairly  well  re- 
tained while  there  is  a  generalized  analgesia.  In  some  of 
Oppenheim's  cases  the  analgesia  was  limited  to  the  hairy 
scalp. 

While  it  is  more  common  for  the  impairment  of  sensibil- 
ity to  be  general  than  for  it  to  be  limited  to  circumscribed 
areas,  such  limitations  are  occasionally  observed.  They  are 
most  frequently  found  on  the  back  and  legs,  but  they  are 
never  sharply  defined  like  the  local  ancesthetic  areas  of 
hysteria.  Even  in  the  localized  areas  of  anesthesia  occur- 
ring in  these  rare  forms,  the  sensibility  to  any  of  the  various 
forms  of  stimuli  is  rarely  completely  abolished.  It  is  dimin- 
ished rather  than  lost,  and  the  areas  of  diminution  merge  in- 
sensibly into  the  regions  where  sensations  are  better  per- 
ceived. It  is  consequently  very  difficult  to  make  diagrams 
of  anaesthesia  in  these  cases.  The  patients  give  unsatisfac- 
tory and  contradictory  answers,  and  it  is  oftentimes  impos- 
sible to  determine  just  where  the  boundaries  of  the  ancesthetic 
areas  are. 

Symptoms  referable  to  the  special  senses  are  common. 


.334 


FUNCTIONAL   EFFECTS    OF    INJURY. 


of  which  the  most  prominent  are  disturbances  of  vision. 
Nystagmus,  an  important  symptom  in  multiple  sclerosis,  is 
not  infrequently  encountered.  It  is  usually  limited  to  lateral 
movements  and  is  rarel}^  pronounced.  There  may  be  weak- 
ness or  parah'sis  of  one  or  more  of  the  extrinsic  ocular  mus- 
cles, thus  causing  double  vision.  Inequality  of  the  pupils,  as 
well  as  the  failure  of  one  or  both  pupils  to  contract  under 
the  stimulation  of  light  have  also  been  recorded.  The 
condition  of  the  pupils  is  essentially  different  from  that 
found  in  simple  traumatic  neurasthenia  in  which  the  dilata- 
tion and  the  quick  response  to  light  and  the  alternating  con- 
traction and  dilatation  are  frequent.  There  is,  in  many 
■cases  of  the  unclassified  forms,  some  slight  limitation  of 
the  visual  fields.  Optic  atroph}-  has  been  rarely  observed. 
Case  X,  of  Oppenheim's,  apparently  developed  atrophy  of 
the  optic  nerve  as  a  result  of  a  railway  accident.  The  his- 
tory of  the  case,  briefly  told,  is  as  follows  : 

A  man,  forty-eight  years  of  age,  received  in  a  railway  accident 
severe  injuries  of  the  back  of  the  head  and  (probably)  of  the  back. 
He  was  rendered  temporarily  unconscious,  but  soon  came  to  him- 
self and  helped  in  clearing  away  the  wreck.  From  that  time  on- 
ward he  complained  of  pain  in  the  back  of  the  head  and  a  tired 
feeling  in  the  back  and  a  constantly  increasing  numbness  and 
weakness  of  the  whole  body.  A  year  after  the  accident  the  sight 
in  the  right  eye  became  impaired.  The  patient  was  first  examined 
bv  Oppenheim  two  years  after  the  accident.  The  symptoms  at 
that  time  consisted  of  depression,  anxiety,  diminution  of  intellec- 
tual power,  dizziness,  and  attacks  of  unconsciousness.  The  visual 
field  for  the  left  eye  was  normal,  but  the  right  visual  field  was  con- 
siderably contracted.  The  right  optic  nerve,  seen  with  the  oph- 
thalmoscope, showed  a  pallor  of  the  whole  papilla  and  a  narrow- 
ing of  the  retinal  vessels. 

He  was  examined  again  after  two  years.  None  of  the  symp- 
toms had  improved  and  some  had  grown  worse.  The  patient  was 
very  depressed  and  wished  to  be  alone.  There  were  occasional 
temporary  losses  of  consciousness,  the  exact  nature  of  which  are 
not  evident  from  the  history.  The  visual  impairment  was  more 
marked  than  at  the  previous  examination,  and  the  optic-nerve  atro- 


UNCLASSIFIED    FORMS. 


335 


phy  had  become  pronounced,  especially  on  the  temporal  side. 
There  was  a  trempr  which  had  many  characteristics  in  common 
with  the  tremor  of  multiple  sclerosis.  The  speech  was  thick- 
There  were  various  disturbances  of  sensory  function. 

Next  to  vision,  hearing  is  the  most  frequently  affected  of 
any  of  the  special  senses  in  the  unclassified  forms.  There 
may  be  dizziness,  subjective  auditory  disturbances,  such  as 
buzzing-  and  ringing  in  the  ears  and  other  annoyances  sim- 
ilar to  those  observed  in  traumatic  neurasthenia.  Diminu- 
tion of  hearing  is  more  frequently  observed  than  the  hyper- 
sensitiveness  of  the  auditory  apparatus  which  is  common 
in  neurasthenia.  It  may  affect  one  ear  more  than  the 
other,  or  there  may  be  a  comparative  deafness  on  both 
sides. 

Taste  and  smell  are  rarely  abolished.  If  these  senses  are 
affected  at  all,  there  is  usually  nothing-  more  than  a  slipfht 
diminution  of  their  functions. 

The  general  symptoms  resemble  those  of  traumatic 
neurasthenia.  The  sleep  is  interrupted  and  disturbed  by 
bad  dreams.  The  patients  often  have  the  grayish,  lifeless 
■color  of  the  skin  commonly  seen  in  chronic  nervous  disease. 
The  appetite  is  poor,  and  there  may  be  a  variety  of  gastric 
disturbances.  The  bowels  are  constipated.  Nutritional 
•disturbances  are  often  well  marked.  The  patients  lose  in 
weight  and  sometimes  become  considerably  emaciated.  The 
vascular  symptoms  are  not  constant.  The  heart  may  remain 
apparently  normal  in  structure  and  function  ;  in  some  cases 
there  is  a  persistent  tachycardia,  and  there  may  eventually 
appear  evidences  of  hypertrophy  and  dilatation  of  the  heart. 
The  urine  shows  no  characteristic  changes.  If  there  is 
a  marked  degree  of  arterio-sclerosis,  the  urine  may  be 
pale  and  of  lowered  specific  gravity.  Sexual  desire  and 
power  are  very  constantly  diminished  and  may  be  entirely 
lost. 

Pathology. — From  the  complexity  and  peculiar  character 


336  FUNCTIONAL   EFFECTS   OF    INJURY. 

of  their  symptoms,  and  from  the  absence  of  any  definite 
knowledge  regarding  their  pathology,  it  seems  to  me  more 
advisable  to  simply  record  the  occurrence  of  such  cases, 
without,  for  the  present  at  least,  claiming  that  they  all  have  a 
common  pathology,  or  without  insisting  too  strongly  upon 
what  the  most  probable  nature  of  their  pathology  is.  Some 
of  the  cases  may  owe  their  symptoms  to  scattered  foci  of 
morbid  tissue  change  in  the  brain  and  perhaps  the  spinal 
cord,  such  as  occur  in  the  brain  in  cerebral  endarteritis,  or  in 
the  whole  cerebro-spinal  axis  in  multiple  sclerosis.  Most  of 
the  symptoms  have  occurred  in  men  who  are  in  the  middle 
or  later  decades  of  life,  a  time  when  degeneration  of  the  vas- 
cular system  is  encountered  with  particular  frequency.  Two 
autopsies  (Sperling  and  Kronthal,  Bernhardt  and  Kronthal), 
made  upon  patients  who  died  during  the  period  when  these 
grave  symptoms  were  marked,  have  disclosed  thickened  ves- 
sels, with  areas  of  degeneration  in  the  cerebro-spinal  axis.  It 
seems  more  reasonable  to  suppose,  however,  that  in  these 
cases  the  injury  added  activity  to  a  process  already  existent, 
rather  than  that  it  caused  a  sclerosis  of  vessels  which  were 
previously  healthy. 

The  probability  and  possibility  of  the  occurrence  of  intra- 
cranial or  intraspinal  injury,  without  there  being  any  reason 
to  suspect  gross  contusions,  lacerations,  or  haemorrhage,  has 
already  been  discussed  in  preceding  pages. 

There  can  be  no  doubt  but  that  minute  and  multiple 
lesions  may  acutely  occur  in  the  brain  as  a  result  of  injury, 
and  that  they  may  furnish  the  general  evidences  of  cerebral 
commotion,  without  indicating  which  portions  of  the  brain 
are  chiefiv  affected.  Of  the  nature  of  these  lesions  we  are 
ignorant,  though  it  is  probable  that  the  larger  number  of 
them  are  hgemorrhagic.  That  such  lesions  (see  case  on  page 
82)  may  occur  in  the  spinal  cord  without  causing  the  death 
of  the  patient  still  remains  to  be  proved,  although  there  is 
reason  to  suppose  that  they  can. 


UNCLASSIFIED   FORMS. 


337 


The  existence  of  disseminated  areas  of  hsemorrhage  seems 
the  most  plausible  pathological  explanation  for  the  types 
which  present  the  exaggerated  forms  of  tremor  and  marked 
increase  of  reflex  activity,  with  notable  inhibition  of  psychi- 
cal function. 

In  other  instances  it  seems  as  though  hysterical  and  or- 
ganic symptoms  occurred  together.  Also  many  of  the  cases 
of  Oppenheim,  in  which  the  symptoms  both  of  neurasthenia 
and  hysteria  occur  together  in  severe  degrees,  may  be 
accounted  for  by  the  simultaneous  existence  of  those  two 
disorders. 

It  is  probable  that  it  will  some  day  be  possible  to  make 
the  group  of  unclassified  forms  more  exclusive.  Some  of 
the  cases  may,  when  our  clinical  and  pathological  knowledge 
is  more  advanced,  be  enrolled  as  variations  of  some  organic 
disorders  which  to-day  are  but  imperfectly  understood ; 
others  may  be  shown  to  be  the  results  of  too  long  exhaustion 
of  nerve  cells,  and  still  others  may  be  found  to  be  consist- 
ent with  the  clinical  course  of  the  multiform  psychosis 
hysteria. 

From  the  observation  of  the  profound  nervous  disturb- 
ances which  result  after  physical  injury  in  heavy  drinkers, 
and  in  persons  whose  vascular  systems  are  in  advanced 
stages  of  degeneration,  I  have  become  convinced  of  the 
force  of  Saenger's  suggestion  that  some  of  these  forms 
may  be  properly  regarded  as  owing  their  existence  to 
organically  degenerated  nervous  systems  quite  as  much 
as  to  the  accidents  which  are  supposed  to  have  caused 
them. 

Diagnosis. — The  diagnosis  of  the  unclassified  forms  is  a 
diagnosis  by  exclusion.  It  can  only  be  made  when  the  symp- 
toms are  of  a  character  to  prevent  them  from  being  regarded 
as  surely  indicative  of  organic  disease,  or  when  they  present 
distinct  variations  from  the  more  common  types  of  the  func- 
tional nervous  disorders  which  follow  accidents. 


338  FUNCTIONAL   EFFECTS   OF    INJURY. 

As  has  been  said,  it  seems  highly  improbable  that  all  of 
the  cases  which  must  for  the  present  remain  unclassified  have 
a  common  pathology.     The  symptoms  present  too  wide  a 
variation  to  make  such  a  supposition  tenable.     The  mental 
state  of  these  cases  may  be  nearly  normal,  or  it  may  be  that 
of  depression,  or  intellectual  power  may  be  so  much  dimin- 
ished as  to  give  a  picture  similar  to  that  of  senile  dementia. 
The    motor   disturbances  also   vary  greatly.     In  the   cases 
which  most  closely   resemble  multiple  sclerosis  the  symp- 
toms are  rarely  identical  with  those  commonly  observed  in 
multiple  sclerosis.     In  the  unclassified  forms  also  diplopia  is 
uncommon,  nystagmus  is  only  slight,  and  the  gait  has  not  the 
marked  spastic  character  of  multiple  sclerosis.     In  the  group 
of  cases  described   by  Nonne,  the  motor  symptoms  differ 
essentially  from  the  motor  symptoms  of  any  disease  hitherto 
described.      The    sensory    disturbances    of   the    unclassified 
forms  resemble  those   of    hysteria,   but   thej^  also  differ  in 
essential  particulars  from  the  hysterical  anaesthesias  which 
are  commonly  met  with.    Consequently,  when  we  assign  any 
given  case  of  nervous  disease  following  injury  to  the  category 
of  unclassified  forms,  we  can  go  no  further  than  to  say  that  the 
case  is  one  of  severe  nervous  disorder.    We  can  not  definitely 
specify  upon  what  pathological  basis  it  rests,  or  by  what  the- 
ory its  symptoms  may  best  be  explained.     Nevertheless,  al- 
though the  diagnosis  can  not,  for  the  present,  be  precise,  it  is 
usually  easy  to  see  that  the  patient  is  suffering  from  an  affec- 
tion more  serious  than  neurasthenia  or  hysteria  are  generally 
supposed  to  be.     The  general  appearance  and  manner,  and 
the  exaggerated  character  of  many  of  the  symptoms,  indicate 
that  there  exists  pronounced  disturbance  of  nervous  function. 
Until  the  existence  of  these  forms  becomes  more   familiar 
to  physicians,  many  of  these  patients  will  continue  to  be  re- 
garded as  simulators.     Such  an  opinion  is  manifestly  unjust, 
as  has  been  amply  shown  by  the  long  periods  of  time  during 
which  the  symptoms  have  frequently  remained  practically 


UNCLASSIFIED    FORMS.  ;  330, 

unchanged,  and  in  many  cases  the  entire  absence  of  any 
motive  for  simulation.  For  certainty  of  diagnosis  it  is  usu- 
ally necessary  for  the  injured  person  to  be  constantly  under 
observation  for  a  considerable  length  of  time.  It  is  only  by 
such  means  that  error  can  be  avoided  in  the  diagnosis  of  dis- 
orders whose  pathology  and  symptomatology  are  so  uncer- 
tain and  so  variable. 

Prognosis. — Of  all  the  factors  which  are  concerned  in  a 
consideration  of  these  unclassified  forms,  the  most  secure 
place  is  held  by  prognosis.  It  is  a  fairly  well-established 
fact  that  few  of  these  cases  recover  completely.^  In  trau- 
matic neurasthenia  most  of  the  patients  eventually  return  to 
work,  and  in  traumatic  hysteria  the  individual  manifestations 
vanish,  leaving  the  patient  apparently  well,  although  com- 
monly branded  with  some  of  the  hysterical  stigmata.  But 
it  is  a  fact  common  to  all  observers  that  the  patients  who- 
fall  within  the  group  of  unclassified  forms  are  only  occa- 
sionally able  to  resume  all  the  duties  which  the  disorder 
obliged  them  to  lay  aside.  Most  commonly  the  symptoms 
attain  a  certain  degree  of  development  and  then  remain  sta- 
tionary. The  patient  gets  neither  permanently  better  nor 
rapidly  worse.  By  rest  and  quiet  he  may  seem  to  improve,, 
but  any  injurious  influence,  such  as  excitement  "or  fatigue, 
or  attempts  to  work,  cause  the  disturbances  to  return  with 
their  former  or  with  an  increased  intensity.  Some  of  the 
patients  get  progressively  worse  and  die,  without  any  cause, 
other  than  the  effect  of  the  accident,  becoming  apparent.  In 
several,  suicide  has  been  reported  as  the  cause  of  death.  A 
good  many  patients  become  eventually  demented,  or  show 
evidence  of  other  forms  of  mental  disease.  Cases  have  been 
reported  as  chronic  lunatics  which  had  previously  been  re- 
garded as  simulators. 

The  prognosis  as  to  recovery  is  consequently  very  bad. 
The  prognosis  as  to  duration  or  as  to  life  must  necessarily 
vary  with  the  individual  case. 


^  .Q  FUNCTIONAL   EFFECTS   OF    INJURY. 

Bibliography. 

Bernhardt  and  Kronthal,  Fall  von  sog.  traum.  Neuros.  mit 
Sect.  Bef.     Neurolog.  Cblatt.,  1890,  No.  4. 

Crocq,  Les  nevroses  traumatiques.     Brussels,  1896. 

Dana,  The  Traumatic  Neuroses.  Hamilton  s  System  of  Legal 
Medicine,  New  York,  1894. 

Knapp,  Traumatic  Sclerosis.  Text-book  of  Nervous  Diseases  by 
American  Authors,  Philadelphia,  1895. 

Nonne,  Ueber  pseudospastische  Parese  mit  Tremor  nach 
Trauma.     Neurolog.  Cblatt..,  1897,  Nos.  20  and  21. 

Saenger,  Die  Beurtheilung  der  Nervenerkrankungen  nach  Un- 
fall.     Stuttgart,  1896. 

Sperling  and  Kronthal,  Eine  traum.  Neurose  mit  Sect.  Befund. 
Neurolog.  Cblatt.,  1889,  Nos.  11  and  12. 


PART    III. 

MALINGERING. 

At  the  present  time  it  is  a  rule,  with  few  exceptions,  that 
persons  who  suffer  real  or  supposed  injury  in  railway  or 
other  accidents  demand  compensation  from  the  companies 
or  individuals  responsible.  Mr.  Lawrence  Godkin,  in  Ham- 
ilton's System  of  Legal  Medicine,  states  that  "  probably  half 
the  jury  cases  tried  in  the  courts  of  the  State  of  New  York 
alone  in  any  one  year  are  actions  for  personal  injuries  re- 
sulting- from  alleged  negligence." 

Mr.  E.  Parmelee  Prentice  has  recently  examined  the  rec- 
ords of  the  Chicago  courts  which  have  jurisdiction  of  these 
cases.  The  results  are  somewhat  startling.  He  says :  "  In 
1875  there  were  altogether  about  two  hundred  personal-injury 
suits  pending  in  Cook  County.  During  the  first  six  months 
of  1890  the  number  of  these  suits  brought  in  Cook  County 
was  346,  the  total  damages  claimed  being  $2,814,860.  Dur- 
ing the  corresponding  six  months  in  1896  the  number  of 
such  suits  brought  in  Cook  County  was  893,  and  the  total 
amount  of  damages  claimed  was  $13,510,000.  It  would  be 
reasonable  to  assume  from  these  figures  that  there  are  now 
pending  in  Cook  Count}^  3,600  of  these  cases,  and  that  the 
damages  claimed  are  between  fifty  and  sixty  million  dollars." 
It  is  needless  to  add  that  this  enormous  increase  is  out  of 
all  proportion  to  the  increase  in  the  number  of  accidents. 

As  is  well  known,  the  number  of  suits  which  come  to 
trial  forms  only  a  small  fraction  of  the  total  number  of  claims 

that  are  entered.     Mr.  Prentice  estimates  that  for  each  claim 

23  341 


342 


MALINGERING. 


that  appears  in  court  it  is  probable  that  eight  or  ten  claims 
are  settled  without  suit. 

The  chances  of  successful  issue,  which  are  notoriously 
good,  seem  to  be  the  most  prominent  consideration  in  bring- 
ing claims  for  damages.  The  extent  of  injury,  or  the  so- 
cial position  of  the  claimant,  are  matters  of  secondary  im- 
portance. The  larger  number  of  claims  are  brought  for 
trivial  injuries,  and  among  the  claimants  may  be  found  the 
poor  and  the  rich,  the  capitalist  and  the  pauper,  men  of  all 
professions,  of  all  creeds,  and  of  all  classes  of  society.  An 
injury  received  through  another's  negligence  has  come  to  be 
regarded  as  capital,  which  is  to  be  converted  as  soon  as  pos- 
sible into  cash.  This  view  has  received  judicial  recognition 
in  Illinois,  for  by  a  recent  decision  of  the  Supreme  Court  of 
that  State  a  claim  for  personal  injuries  is  property,  which 
may  be  put  on  the  market  and  transferred  or  trusteed. 

The  larger  portion  of  the  population  is  thoroughly  cog- 
nizant of  its  rights,  and  loses  little  time  after  the  accident  in 
calling  the  attention  of  the  responsible  parties  to  the  injuries 
which  have  been  received.  If  no  thought  of  financial  recom- 
pense occurs  to  the  injured  person  at  first,  this  is  an  omission 
which  will  soon  be  remedied,  either  by  sympathizing  friends 
or  by  persons  experienced  in  the  value  of  a  personal  injury  as 
the  basis  for  a  damage  claim.  The  press  exerts  an  important 
influence  upon  the  number  of  claims  and  suits  for  damages. 
It  is  especially  noticeable  in  rural  districts,  where  the  publi- 
cation of  a  large  verdict  rendered  in  a  negligence  case  is  com- 
monly followed  by  a  very  appreciable  increase  in  the  number 
of  personal-injuries  claims  brought  in  the  neighborhood  of 
the  original  accident.  This  is  partly  due  to  the  increased  at- 
tention given  to  injuries  when  it  becomes  generally  known 
that  they  may  be  so  easily  turned  into  financial  benefit,  and 
partly  because  the  lawyers  who  make  a  specialty  of  scanning 
the  papers  in  search  of  casualties  have  their  attention  thus 
called  to  a  promising  field  for  their  activities. 


INDUCEMENTS   TO    MALINGERING.  343 

Any  press  mention  of  an  accident  occurring  in  a  large 
city  is  sufficient  to  secure  for  the  injured  person  an  abun- 
dance of  gratuitous  and  unsolicited  counsel.  A  man  was 
recently  injured  in  New  York  late  in  the  afternoon.  Be- 
fore eleven  o'clock  the  next  morning  eight  lawyers  had 
called  at  the  hospital  to  see  him.  The  last  hours  of  the 
unfortunate  man  were  passed  in  listening  to  the  arguments 
of  the  attorneys  who  were  going  to  secure  damages  for  him, 
had  they  gotten  the  chance. 

The  prosecution  of  personal-injury  suits  has  become  a 
systematized  business.  Mr.  Prentice  says  that  many  law 
firms  and  brokers  employ  "  runners,"  who  have  business 
relations  with  saloon-keepers,  policemen,  and  surgeons  living 
in  the  parts  of  the  city  where  accidents  are  frequent.  The 
runners  are  constantly  on  the  lookout  for  accidents,  and  as 
soon  as  one  occurs  they  discover  it  themselves,  or  are  noti- 
fied by  their  associates,  and  lose  no  time  in  trying  to  persuade 
the  injured  person  to  intrust  his  claim  to  the  firms  or  brokers 
whom  they  represent. 

In  New  York  city  the  value  of  information  regarding  an 
accident  is  so  generally  recognized  that  witnesses  carry  the 
news  voluntarily  to  the  offices  of  "  ambulance  chasers,"  sat- 
isfied with  the  small  fee  which  they  are  almost  certain  of 
receiving  in  return  for  their  services. 

It  is,  of  course,  simple  justice  that  persons  who  have 
been  injured  through  the  negligence  of  others  should  receive 
reimbursement  for  the  losses  entailed  by  absence  from  their 
business,  and  that  they  should  be  compensated  for  the  suffer- 
ing they  have  been  made  to  pass  through,  as  well  as  for  any 
resulting  disability.  And  if,  as  sometimes  happens,  the  in- 
jured person  is  ignorant  of  his  rights  in  such  matters,  it  is 
essential  and  proper  that  these  rights  should  be  explained  to 
him.  Nevertheless,  although  the  larger  number  of  actions 
which  are  brought  for  personal  injuries  are  in  all  probability 
based  upon  some  actual,  though  often  slight,  loss  of  health, 


344 


MALINGERING. 


it  is  inevitable,  with  the  enormous  increase  in  recent  years 
in  the  number  of  accidents,  that  many  cases  which  appear  in 
the  courts  be  attended  with  a  certain  amount  of  absolute 
fraud.  And  the  number  of  persons  who  demand  compensa- 
tion from  corporations  for  trivial  injuries,  or  whose  claims 
are  absolutely  fraudulent,  and  who,  either  by  compromise  or 
by  failure  to  prosecute,  or  for  any  other  reason,  do  not  ap- 
pear in  the  court,  must  be  very  large  indeed. 

The  enormous  sums  paid  every  year  by  large  corpora- 
tions as  indemnity  for  personal  injuries  renders  the  tempta- 
tion to  this  kind  of  fraud  very  strong. 

The  general  claim  agent  of  a  Western  railway  whose  sys- 
tem covers  about  five  thousand  miles  told  me  that  in  the 
year  1896  the  company  paid  $350,000  in  personal-injury 
claims  alone.  This  sum  was  entirely  exclusive  of  the  judg- 
ments in  cases  which  were  brought  to  trial  and  which  were 
decided  against  the  company.  Another  large  American 
railway  pays  between  $200,000  and  $400,000  damages  every 
year  for  personal  injuries. 

It  is,  furthermore,  a  generally  recognized  fact  that  cor- 
porations prefer  to  settle  small  claims,  even  when  convinced 
that  they  are  fraudulent,  to  defending  suits.  They  are  forced 
to  adopt  the  policy  of  settling  claims  rather  than  of  letting 
them  go  to  trial,  from  the  well-known  attitude  of  juries 
toward  the  defendant  when  the  latter  happens  to  be  a  cor- 
poration. It  is  often  flagrantly  apparent  in  such  trials  that 
the  jury,  in  reaching  a  verdict,  has  concerned  itself  less 
with  the  evidence  than  with  a  consideration  of  the  rela- 
tive financial  resources  of  the  plaintiff  and  of  the  defendant. 
This  was  recently  shown  in  Brooklyn,  when  Justice  Wilmot 
M.Smith  set  aside  the  verdict  of  $11, 000  obtained  by  Christian 
F.  Stark  against  the  City  of  Brooklyn  and  the  South  Brooklyn 
Terminal  Railroad  Company.  Stark  sued  for  damages  for 
personal  injuries  received  by  falling  down  an  embankment 
at  Thirty-eighth  Street.     In  a  previous  trial  Stark  received 


SPECULATION    IN   DAMAGE   CLAIMS. 


345 


a  verdict  of  $10,000,  which  also  was  set  aside.  Justice  Smith 
said  :  "  Prejudice  or  passion  must  have  influenced  a  verdict 
so  at  variance  with  a  result  which  should  have  been  reached 
upon  a  sober,  impartial,  and  rational  consideration  of  the  evi- 
dence. A  verdict  of  a  jury  should  not  be  disturbed  unless 
to  allow  it  to  stand  would  result  in  a  clear  failure  of  justice. 
I  set  aside  the  verdict  because  of  a  settled  conviction  in 
my  mind  that  to  allow  it  to  stand  would  be  a  serious  reflec- 
tion upon  the  administration  of  justice,  and  a  confession  that 
the  courts  do  not  furnish  a  tribunal  to  which  all  citizens  may 
repair  with  confidence  that  their  contentions  will  receive 
rational  and  impartial  consideration." 

As  long-  as  prejudice,  in  the  minds  of  the  jury,  against 
corporations  can  be  counted  upon,  the  temptation  to  bring 
damage  suits  upon  insufficient  grounds  will  remain  very 
great.  The  inducements  for  exaggeration  and  deceit  which 
are  brought  about  by  these  means  are  furthered  by  the 
speculation  in  damage  claims,  which  has  become  so  serious 
a  sociological  problem.  Many  negligence  cases  are  taken 
on  the  contingent-fee  plan  by  lawyers  who  associate  with 
themselves  self-constituted  medical  "  experts."  The  lawyer 
supplies  the  witness,  the  doctor  formulates  his  opinion,  and 
the  result  is  one  of  two :  The  corporation  settles,  if  it  can  do 
so  on  not  too  extravagant  terms  ;  or  it  decides  to  "  fight  "  ; 
it  then  engages  in  an  unequal  contest. 

In  this  way  many  claimants  and  plaintiffs  receive  much 
larger  sums  than  any  to  which  their  injuries  entitle  them,  or 
are  paid  by  the  company  even  when  they  are  entitled  to  no 
compensation  whatsoever. 

The  rectification  of  this  question  lies  with  the  corpora- 
tions themselves  and,  in  a  way,  with  the  medical  profession. 

By  showing  themselves  more  zealous  in  promoting  the 
comfort  and  privileges  of  their  patrons,  and  by  insisting 
upon  more  courteous  behavior  on  the  part  of  employees, 
transportation  and  other  companies  which  have  to  do  with 


346 


MALINGERING. 


large  numbers  of  the  public,  have  their  surest  means  of 
gaining  the  good  will  of  the  community,  and  of  thus  doing 
away  with  the  general  prejudice  against  them  which  be- 
comes so  apparent  when  they  engage  in  litigation  against 
private  individuals. 

The  part  to  be  done  by  the  medical  profession  will  only 
be  possible  when  legislation  has  provided  an  answer  to  the 
vexed  question  of  experts.  At  present,  when  there  is  no 
legal  criterion  by  which  the  value  of  a  medical  opinion  may 
be  estimated,  the  testimony  of  a  charlatan  may  carry  as  much 
weight  to  the  minds  of  a  jury  as  that  of  a  physician  who  has 
shown  himself  skilled  in  his  subject.  It  is  the  contradic-- 
tion  of  professional  opinion  in  the  witness  chair  which  has 
brought  medical  expert  testimony  into  disrepute,  and  which 
has  caused  it  to  be  so  often  regarded  as  of  questionable  value 
as  evidence. 

With  the  existing  state  of  affairs  it  is  not  surprising  that 
the  feigning  of  disease  alleged  to  be  the  result  of  accidents, 
or  the  exaggeration  of  symptoms  due  to  actual  injuries,  are 
difficulties  against  which  corporations  must  constantly  con- 
tend and  are  means  by  which  they  are  not  infrequently  de- 
frauded ;  yet  from  a  purely  medical  point  of  view  it  should 
be  generally  easy  to  unmask  the  malingerer. 

Simulation  is  of  necessity  limited  chiefly  to  diseases  of 
the  nervous  system.  In  visible  physical  injuries  there  is  little 
chance  for  fraud.  Fractures,  dislocations,  and  similar  purely 
surgical  affections  can  not  be  successfully  feigned.  Few  care 
to  voluntarily  injure  themselves  in  a  way  to  cause  any  misin- 
terpretation. Instances  of  serious  wounds  self-inflicted  by 
malingerers  may  be  found  in  medical  and  criminal  annals,  but 
in  these  cases  the  underlying  motives  were  stronger  than 
the  hope  of  financial  reward.  In  litigation  cases  self-disfig- 
urement is  limited  to  abrasions  or  similar  slight  personal  in- 
juries, of  which  the  trivial  character  is  readily  apparent  and 
about  the  means  of  whose  production  there  can  be  no  great 


EXAGGERATION   OF   SYMPTOMS   ACTUALLY   PRESENT. 


347 


doubt.  With  the  nervous  system  the  case  is  different. 
Nervous  structure  is  hidden  and  protected  ;  no  part  of  it 
can  be  felt,  and  the  optic  nerve  is  the  only  part  of  it  that 
can  be  seen,  and  then  only  by  means  of  the  ophthalmoscope. 
In  popular  opinion,  nervous  function  is  indefinite,  and  nerv- 
ous diseases  obey  no  recognized  laws. 

It  is  generally  known  that  participators  in  accidents  often 
receive  large  sums  of  money  for  injuries  to  the  nervous  sys- 
tem, although  no  visible  injury  be  sustained  and  although 
the  claimants  present  no  symptoms  more  definite  than  those 
popularly  supposed  to  constitute  "  nervous  prostration." 
Consequently  it  is  to  the  imitating  of  diseases  of  the  nervous 
system  that  the  simulator  naturally  turns,  and  it  is  with 
them  that  he  has  the  greatest  chance  for  success.  Neurol- 
ogy is  the  most  recently  developed  branch  of  clinical  medi- 
cine, and  is  the  one  least  familiar  to  physicians  generally. 
As  the  study  of  it  becomes  more  popular,  successful  simula- 
tion will  become  more  rare ;  for,  notwithstanding  the  com- 
plexity and  minuteness  of  the  architecture  of  the  nervous 
system,  and  the  mystery  which  must  ever  surround  nervous 
function,  nervous  disease  causes  characteristic  and  fairly 
constant  symptoms.  The  detection  of  simulation  depends 
upon  a  knowledge  of  them  on  the  part  of  the  physician,  and 
the  inability  on  the  part  of  the  malingerer  to  exaggerate  or 
create  the  products  of  disease. 

Fraud  is  attempted  in  accident  cases  in  three  principal 
wa3^s  : 

I.  Exaggeration  of  symptoms  actually  present.  2.  The 
substitution  of  origin,  or  the  allegation  that  pre-existing  dis- 
ease was  caused  by  the  accident.     3.  Entire  simulation. 

I.  Exaggeration  of  Symptoms  Actually  Present. 

Of  the  different  ways  the  first  is  by  far  the  most  common. 
It  is  rarely  seen  in  organic  injuries.  The  patient  who  has 
sustained  a  fracture  of  the  skull  or  an  injury  to  the  spinal 


348 


MALINGERING. 


cord  is  too  seriously  hurt  to  think  about  exaggerating  his 
symptoms.  It  would  hardly  seem  possible  that  uncompli- 
cated injury  to  one  of  the  peripheral  spinal  nerves  could  in 
these  days  be  so  construed  as  to  serve  as  the  basis  for  a 
claim  that  the  spinal  cord  had  been  injured,  and  that  as  a 
result  the  patient  was  suffering  from  incurable,  progressive, 
and  ultimately  fatal  spinal  disease.  Yet  such  a  case  has 
recently  come  to  my  knowledge.  The  musculo-spinal  nerve 
had  been  injured  by  a  blow  which  had  caused  a  peripheral 
and  probably  temporary  weakness  of  the  muscles  supplied 
by  the  nerve.  The  physician  for  the  plaintiff  must  have 
counted  upon  the  incapacity  of  the  experts  for  the  defense 
and  the  gullibility  of  the  jury,  or  else  have  himself  been  very 
ignorant  of  nervous  diseases.  Fortunately,  the  injury  was 
recognized  at  its  true  value. 

It  is  most  commonly  the  functional  conditions,  and  es- 
pecially neurasthenia,  which  are  fraudulently  exaggerated. 
The  number  of  persons  who  appear  before  a  claim  agent 
professing  great  suffering  and  disability,  although  they  know 
that  there  is  little  or  nothing  the  matter  with  them,  is  cer- 
tainly large.  It  is  impossible  to  determine  the  proportion 
of  dishonest  claims,  but  it  is  unquestionably  large  enough  to 
make  the  subject  one  of  the  most  important  in  medical  juris- 
prudence. Many  claimants  allege  injuries  so  trivial  and  so 
obviously  exaggerated,  that  they  are  readily  persuaded  to 
withdraw  the  claim  without  any  medical  examination.  The 
extent  and  frequency  of  exaggeration  in  the  cases  examined 
by  the  corporation  surgeon  must  be  in  part  determined  by 
the  surgeon  himself.  It  is  often  a  matter  very  difficult  to 
decide.  When  there  is  no  question  as  to  the  reality  of  some 
of  the  symptoms,  it  is  frequently  impossible  to  ascertain  just 
how  far  the  real  symptoms  are  voluntarily  magnified.  Al- 
though he  can  not  always  give  reasons  for  his  opinion  which 
prove  satisfactory  to  juries,  an  experienced  surgeon  can 
usually    tell  from    the  appearance    and    manner   of   the    pa- 


EXAGGERATION    OF    SYMPTOMS    ACTUALLY    PRESENT.     34^ 

tient  whether  he  believes  himself  to  be  as  ill  as  he  claims 
to  be. 

But  although  voluntary  and  dishonest  exaggeration  of 
subjective  nervous  symptoms  is  frequent,  it  should  be  re- 
membered that  not  all  neurasthenics  who  may  be  suspected 
of  exaggeration  are  themselves  conscious  of  any  misrepre- 
sentation. What  appears  at  first  sight  as  exaggeration  may 
be  only  a  symptom  of  disease.  This  fact  is  too  little  recog- 
nized outside  of  the  medical  profession.  The  bringing  of 
claims  by  persons  suffering  from  slight  subjective  nervous 
symptoms  has  won  for  the  neurasthenic  among  claim  agents 
and  corporation  lawyers,  the  name  of  swindler  and  extor- 
tioner. It  is  not  surprising  that  a  claim  agent,  whose  medi- 
cal knowledge  must  at  its  best  be  but  superficial,  and  who  is 
so  constantly  a  witness  of  attempted  frauds,  should  be  skep- 
tical as  to  the  justice  of  all  claims  for  injuries  which  can 
not  be  objectively  proved.  He  is  unaware  that  the  same 
kind  of  exaggeration  he  so  often  sees  in  the  claim-bureau  is 
daily  observed  by  physicians  in  cases  which  are  uncompli- 
cated by  "  litigation  symptoms."  As  has  been  stated  in 
previous  chapters,  the  patient  with  traumatic  neurasthenia, 
even  when  he  has  no  claim  to  bring,  describes  his  symp- 
toms as  more  severe  than  there  is  any  reason  to  suppose 
they  are. 

A  person  who  has  become  neurasthenic  is  tired  and 
weak.  However  robust  or  careless  he  may  previously  have 
been,  exhaustion  of  the  nervous  system  has  rendered  him 
easily  fatigued  and  worried,  and  fearful  about  himself.  By 
the  immediate  discomfort  they  occasion,  and  by  arousing 
fears  of  trouble  in  the  future,  the  pains  he  feels  are  double 
causes  of  suffering.  He  can  not  keep  his  mind  from  his 
own  sufferings,  and  thereb}^  makes  himself  worse,  in  accord- 
ance  with  the  law  of  psychology  that  attention  causes  an 
intensification  of  sensations.  Could  he  divert  his  thouofhts 
to  other  channels  he  would  be  on  the  highroad  to  recovery. 


350 


MALINGERING. 


An  individual  who  is  occupied  and  who  has  neither  time 
nor  inclination  to  think  about  his  own  physical  ailments,  is 
not  worried  by  such  trifling  symptoms  as  cause  suffering  to 
a  nervous  man  who  has  given  up  his  work  and  who  thinks 
only  about  himself.  The  tendency  of  introspection  which 
is  a  prominent  feature  in  neurasthenia,  and  which  is  invari- 
ably detrimental  to  recovery,  is  very  much  increased  when 
the  financial  question  enters. 

Furthermore,  a  person  who  is  claiming  damages  for  in- 
juries can  not  afford  to  make  light  of  any  symptoms  which 
he  may  observe.  All  the  circumstances  by  which  he  is  sur- 
rounded tend  to  cause  him  to  repress,  until  the  case  is  de- 
cided, any  efforts  on  the  part  of  Nature,  or  of  his  physician, 
directed  to  dispel  the  physical  annoyances  and  suffering  to 
which  he  is  subjected.  By  frequently  rehearsing  his  case  to 
lawyers  and  to  experts  he  comes  to  believe  that  he  is  seri- 
ously injured  ;  by  constantly  bewailing  the  permanency  of  old 
troubles,  or  the  advent  of  new  ones,  he  concludes  that  he 
is  "  ruined  for  life."  The  symptoms  of  a  patient  who  has 
arrived  at  this  stage  are  so  out  of  proportion  to  the  physical 
injuries  he  has  received  that  the  representative  of  the  cor- 
poration which  is  to  settle  for  them  thinks  they  are  volun- 
tarily invented,  when  the  patient  himself  believes  in  their 
reality  absolutely. 

The  discrimination  between  exaggeration  of  this  charac- 
ter, which  is  the  voicing  of  disease,  and  consequently  sin- 
cere, and  the  variety  of  exaggeration  which  is  the  outcome 
of  dishonest  greed,  often  can  not  be  effected  by  the  medical 
aspects  of  the  case  alone. 

As  has  been  said  in  speaking  of  the  S3^mptoms  of  trau- 
matic neurasthenia,  the  disorder,  when  well  marked,  consti- 
tutes a  fairly  typical  clinical  type.  In  such  cases  there  is  an 
agreement  between  the  story  the  patient  tells  and  the  way 
he  looks  and  acts  which  leaves  no  doubt  in  the  physician's 
mind  that  he  is  really  ill.     But  in  mild  cases  the  examiner 


EXAGGERATION   OF   SYMPTOMS   ACTUALLY   PRESENT.    351 

has  to  depend  solely  on  the  patient's  symptoms,  a  means 
none  too  reliable  in  litigation  cases.  It  is  then  usually  im- 
possible to  decide  this  question  from  an  examination  of  the 
patient  alone.  If  a  man  claims  to  have  a  headache,  or  a 
pain  in  the  back,  although  he  may  not  present  the  physical 
appearances  which  ordinarily  accompany  such  disturbances, 
it  is  impossible  to  prove  that  his  head  or  his  back  do  not 
ache.  Even  to  show  him  to  be  a  liar  in  other  ways  would 
not  necessarily  prove  that  he  was  lying  about  these  symp- 
toms. It  is  but  natural  that  the  feigning  of  symptoms  of 
this  character,  which  are  subjective  and  which  do  not 
necessarily  reveal  themselves  by  objective  and  tangible  evi- 
dences, should  prove  a  tempting  bait  to  persons  who  wish 
to  turn  their  presence  in  an  accident  to  good  account,  or  to 
swindlers  who  may  invent  the  history  of  the  accident  as 
w^ell  as  the  symptoms. 

The  decision  as  to  the  merits  of  such  cases  usually  lies 
beyond  the  province  of  the  physician,  and  must  be  decided 
by  means  of  information  from  outside  sources.  It  should 
be  ascertained  if  the  patient  conducts  himself  at  all  times 
in  a  manner  which  is  consistent  with  the  existence  of 
the  symptoms  from  which  he  is  alleged  to  be  suffering ;  it 
he  is  bringing  the  claim  himself,  or  if  he  is  the  victim  of 
*'  speculation."  The  profession  and  social  position  of  the 
claimant  is  not  always  a  valuable  aid  in  arriving  at  a  just 
conclusion.  Physicians,  and  even  the  clergy,  have  been 
known  to  bring  claims  of  more  than  doubtful  justice.  An 
officer  of  a  large  corporation  has  communicated  to  me  the 
case  of  a  priest  who  was  in  a  collision  in  which  he  received 
no  external  injuries  whatsoever,  and  who,  although  experi- 
encing no  ill  effects  immediately  after  the  accident,  brought 
a  claim  against  the  company,  alleging  various  subjective 
nervous  symptoms.  The  man's  occupation  was  of  a  charac- 
ter to  demand  excessive  mental  and  physical  work,  which 
he  has  continued  to  do  without  interruption  since  the  acci- 


oe2  MALINGERING. 

dent.  An  examination  by  a  distinguished  neurologist  two 
years  after  the  accident  failed  to  reveal  any  evidences  of 
organic  disease,  and  while  the  physician  could  not  deny  that 
the  patient  was  still  suffering  from  the  results  of  the  acci- 
dent, he  stated  that  there  was  no  proof  of  injury  other  than 
the  claimant's  own  story. 

The  same  gentleman  told  me  of  a  clergyman  who  was 
struck  in  the  back  by  a  mail  sack,  but  who  received  no  visi- 
ble injury.  He  threatened  suit  for  five  thousand  dollars, 
and  compromised  for  one  hundred  and  fifty  dollars. 

The  question  may  be  one  of  extreme  difficulty.  It  is  one 
thing  to  say  that  there  are  no  evidences  of  disease  discover- 
able, but  it  is  an  entirely  different  matter  to  prove  that  a 
man  does  not  suffer.  When,  however,  the  physician  fails  to 
find  evidence  of  disease,  and  when  it  can  be  proved  that  the 
patient  by  his  daily  life  shows  himself  to  be  strong  and 
active,  there  is  every  probability  that  his  suffering  is  slight 
at  best. 

2.  Substitution  of  Origin. 

The  allegation  that  pre-existing  disease  or  deformity  were 
the  direct  results  of  accident  or  injury  is  a  form  of  fraud  often 
difficult  of  detection.  If  a  person  claims  that  he  was  in 
every  way  normal  prior  to  an  injury,  and  that  only  since  its 
incurrence  have  been  observed  the  symptoms  for  which 
damages  are  claimed,  the  proof  of  this  assertion  depends 
upon  facts  relative  to  his  previous  physical  or  mental  con- 
dition, or,  in  case  such  facts  are  not  obtainable,  or  are  unre- 
liable, upon  whether  the  disability  or  disfigurements  from 
which  he  suffers  are  of  a  character  such  as  may  result  from 
the  kind  of  injury  which  has  been  received.  The  difficulties 
in  obtaining  sufficient  knowledge  of  the  claimant's  previous 
life  is  illustrated  by  a  case  reported  by  Prentice : 

A  corporation  was  presented  with  a  person  apparently  an 
idiot,    his  condition    being  represented   as   the  result  of    a    blow 


SUBSTITUTION    OF   ORIGIN.  353 

on  the  head.  The  company's  attorney  took  the  precaution  of 
having  his  picture  taken.  No  record  of  the  accident  could  be 
found,  and  after  the  man  had  left  the  attorney's  office  he  could 
not  be  found.  The  picture,  however,  was  sent  to  all  parts  of  this 
■country  and  Europe  where  information  might  be  expected ;  de- 
tectives were  employed  in  mines  in  Montana  and  in  cities  on  the 
Atlantic  coast,  with  the  final  result  that  the  defendants'  attorney 
learned  the  man's  birthplace  in  Europe,  discovered  his  name  upon 
the  army  registers,  with  the  record  of  his  physical  condition,  show- 
ing that  his  condition  as  a  youth  had  been  such  as  it  was  when  he 
was  presented  as  a  claimant.  It  was  subsequently  shown  that  he 
had  first  come  to  America  six  months  after  the  accident. 

This  case  illustrates  the  difficulties,  but  still  more  sig- 
nificantly the  importance,  of  obtaining  knowledge  of  the 
preceding  condition  of  the  patient  in  accident  cases.  It  is  a 
necessity  to  which  corporations  are  rapidly  becoming  alive, 
and  for  which  they  are,  as  far  as  possible,  providing.  Most 
corporations  now  demand  a  physical  examination  of  appli- 
cants for  employment.  The  adoption  of  this  rule  is  in  large 
part  due  to  the  unusual  frequency  in  the  past  with  which 
herniae  have  been  alleged  by  employees  to  have  resulted 
from  blows  or  falls.  The  frequency  of  such  claims  was  so 
out  of  proportion  to  the  percentage  of  traumatic  hernise  in 
general  surgical  practice  that  the  companies  concluded  that 
they  often  paid  for  disabilities  which  had  existed  for  a  long 
time  before  the  injury,  and  for  which  they  were  not  respon- 
sible. By  adopting  the  system  of  physical  examination  of 
proposed  employees  they  have  materially  diminished  the 
number  of  unjust  claims  which  are  brought  against  them, 
and  have  at  the  same  time  established  means  for  securing 
valuable  statistics  for  traumatic  surgery. 

It  is,  however,  the  chronic  degenerative  diseases  of  the 
nervous  system  which  are  particularly  liable  to  misconcep- 
tion as  to  the  influence  of  trauma  in  their  causation.  In 
many  of  them  the  evidences  as  to  the  possibility  of  a  trau- 
matic origin  are  still  very  slight,  although  we  are  unable  to 


354 


MALINGERING. 


assert  that  they  can  not  directly  result  from  injury  inde- 
pendently of  the  co-operation  of  other  causes. 

In  traumatic  epilepsy  and  general  paresis,  which  some- 
times develop  in  immediate  sequence  to  blows  on  the  head^ 
it  may  often  require  both  delicacy  of  diagnosis  and  a 
very  full  knowledge  of  the  patient's  condition  prior  to  the 
receipt  of  the  injury,  before  it  is  possible  to  determine  the 
appropriate  causal  value  which  should  be  ascribed  to  it.  As 
has  been  stated,  in  these  diseases  particularly  there  are 
many  opportunities  for  error.  If  a  previously  healthy  person^ 
a  few  weeks  or  months  after  a  fall  on  the  head,  by  which  the 
skull  may  or  may  not  have  been  fractured,  begins  to  have 
convulsive  attacks,  which  at  first  are  localized  to  certain 
muscles,  but  which  may  later  become  general,  it  is  in  entire 
accord  with  our  present  medical  knowledge  to  assume  that 
the  epilepsy  is  traumatic,  and  that  the  patient  would  never 
have  had  the  disease  if  his  head  had  not  been  injured.  Very 
much  more  conservatism  is  necessary  in  ascribing  a  trau- 
matic origin  to  general  paresis  when  it  first  appears  after  a 
head  injury.  It  is  essential  to  have  considerable  evidence 
that  before  the  injury  the  patient  had  been  free  from  any 
symptoms  of  either  of  these  disorders ;  for  epilepsy  fre- 
quently appears  for  the  first  time  in  adolescence  or  in  early 
adult  life,  and  the  fall  on  the  head,  which  is  alleged  to  have 
caused  it,  may  be  the  result  of  the  first  epileptic  attack  ;  in 
general  paralysis,  also,  even  when  there  is  no  question  of  in- 
jury, the  epileptiform  attack  may  be  the  first  symptom 
noticed  by  the  friends  of  the  patient,  and  it  may  be  by  it  that 
attention  is  called  to  the  fact  that  the  patient  had  been  for 
some  time  different  in  many  ways  from  what  he  used  to  be. 
In  such  cases,  of  course,  the  mental  symptoms  are  not  in  any 
way  the  results  of  the  fall.  The  attack  and  the  fall  simply 
form  another  link  in  the  chain  of  symptoms. 

But  if  the  circumstances  of  the  fall  were  such  as  to  make 
it  a  negligence  case,  the  claim  might  be  made  that  the  men- 


SUBSTITUTION   OF   ORIGIN. 


355 


tal  disease  was  traumatic,  and   that  the  fall  was  propter  hoc, 
when  in  reality  it  was  post  hoc. 

If  the  symptoms  of  locomotor  ataxia  or  progressive  mus- 
cular atrophy  are  observed  for  the  first  time  after  an  injury, 
it  is  sometimes  claimed  that  the  injury  was  the  sole  cause  of 
the  disease. 

As  has  been  shown  (page  138),  there  is  no  evidence  that 
locomotor  ataxia  may  be  entirely  due  to  injury.  When 
trauma  is  alleged  as  a  sole  cause,  there  is  a  far  greater  prob- 
ability that  the  disease  had  existed,  perhaps  unperceived, 
before  the  injury.  The  affection  is  always  of  extremely  in- 
sidious onset,  and  is  generally  unfamiliar,  in  the  earlier  stages 
at  least,  to  the  larger  number  of  American  physicians.  These 
facts  should  make  one  chary  of  too  hastily  ascribing  the 
development  of  any  case  to  traumatic  causes  alone. 

Progressive  muscular  atrophy  has  only  infrequently  be- 
come the  subject  of  medico-legal  inquiry.  The  evidence 
necessary  for  the  establishment  of  a  traumatic  origin  of  the 
disease  has  already  been  mentioned  (page  167). 

In  paralysis  agitans  the  chances  of  error  are  fewer.  Cases 
of  paralysis  agitans  which  follow  injury  or  fright  only  ex- 
ceptionally reach  a  rapid  general  development ;  so  that,  if 
a  patient  has  marked  tremor  or  stiffness  of  the  muscles,  or 
characteristic  attitude  or  expression  soon  after  an  accident, 
it  is  highly  probable  that  the  disease  had  existed  before. 

It  must  be  clearly  understood  that  a  person  who  claims 
that  any  of  these  diseases  is  the  direct  result  of  injury 
may  do  so  with  perfect  honesty.  He  may  himself  have 
been  ignorant  of  their  pre-existence.  Thus,  a  patient  of 
Prince's  sued  for  damages,  alleging  that  locomotor  ataxia, 
from  which  he  was  suffering,  was  the  direct  result  of  a  fall 
from  the  back  platform  of  a  railway  car.  The  plaintiff  frankly 
acknowledged  in  the  court  room  that  he  had  suffered  from 
shooting  pains  in  the  legs  of  a  typically  tabetic  character  for 
six  years  previously.     By  this  admission  he  vindicated  him- 


356  MALINGERING. 

self  from  any  suspicion  of  fraud,  but  he  also  g-ave  almost  cer- 
tain proof  that  the.-disease  had  antedated  the  accident. 

There  is  great  opportunity  for  fraud  in  these  cases. 
Dr.  Peterson  has  communicated  to  me  a  case  (already  re- 
ferred to)  of'  progressive  muscular  atrophy  in  which  a 
woman  sued  for  injuries  received  by  a  blow  on  the  head 
caused  by  the  falling  of  a  revolving  fan.  The  plaintiff 
alleged  that  since  the  accident  she  was  nervous,  tremulous, 
and  could  not  sleep  well.  She  was  examined  b}^  the  defend- 
ant's physician,  who  failed  to  observe  the  atrophy  and  loss 
of  power  in  the  hands,  and  apparently  found  symptoms  of 
nothing  more  serious  than  simple  traumatic  neurasthenia. 
After  twelve  months,  when  the  case  came  to  trial,  the  plain- 
tiff's counsel  frankly  admitted  that  his  client  had  suffered  for 
several  years  from  a  chronic  and  incurable  nervous  disease 
which  had  been  rendered  worse  b}^  the  accident.  There 
was,  of  course,  no  attempt  at  deception ;  but  nothing  could 
illustrate  better  the  possibility  of  fraud  by  claiming  that  pre- 
existing disease  had  been  caused  by  the  traumatism.  The 
time  elapsing  between  the  receipt  of  the  injury  and  the 
trial  was  long  enough  for  progressive  muscular  atrophy  to 
develop,  and  had  this  patient  been  unscrupulous,  and  her 
physician  dishonest,  she  could  undoubtedly  have  recovered 
a  large  sum  on  the  complaint  that  the  chronic  spinal  disease 
had  been  the  direct  result  of  trauma. 

What  has  been  said  concerning  the  possible  pre-existence 
of  the  chronic  organic  diseases  of  the  nervous  system  may 
be  repeated,  with  certain  modifications,  for  the  functional 
nervous  disorders.  It  is  very  essential  to  know  something 
about  the  previous  history  of  the  patient.  Neurasthenia 
very  commonly  develops  in  persons  who  had  given  no 
symptoms  before  the  accident,  but  the  fact  that  they  were 
well  before  should  be  proved.  It  is  particular!}^  important 
to  know  if  there  had  been  no  manifestations  of  hysteria 
before   the   appearance  of  the  particular  ones  which  were 


SIMULATION. 


357 


complained  of  soon  after  the  accident.  Thus,  in  Bremer's 
case  (page  301)  of  astasia-abasia,  the  woman  who  sued  for 
damages,  alleging  that  the  paralysis  of  the  legs  would  not 
have  occurred  had  she  not  been  in  an  elevator  accident,  was 
shown  to  have  been  for  years  a  victim  of  various  hysterical 
accidents,  and  to  have  given  many  proofs  of  an  extremely 
disordered  mental  state. 

3.  Simulation. 

Much  confusion  has  arisen  from  an  indefinite  tise  of  the 
term  simulation.  It  has  been  made  to  apply  to  cases  which 
were  exaggerated  as  well  as  to  those  which  were  'entirely 
created.  It  will  be  used  here  as  a  designation  for  those  cases 
only  in  which  there  is  no  foundation  in  fact  for  the  symp- 
toms which  are  alleged. 

Frequency. — It  is  now  generally  admitted  by  railway 
officials,  and  believed  by  neurologists,  that  it  is  not  very 
common  for  persons  who  have  no  symptoms  at  all  to  simu- 
late disease  as  a  result  of  accidents,  on  account  of  which- 
they  demand  compensation.  Simulation  of  all  kinds  is  fre- 
quent in  armies,  in  prisons,  and  in  institutions  for  insane 
criminals,  and  in  the  earlier  periods  of  the  history  of  trau- 
matic nervous  affections  it  was  thought  to  be  very  frequently 
associated  with  them.  Riegler  was  the  first  to  observe  the 
great  increase  in  the  number  of  railway  claims  after  the 
passage  in  Germany  of  a  law  by  which  injured  persons  were 
to  receive  payments,  graded  in  amounts  in  accordance  with 
what  they  had  previously  earned,  for  the  time  they  were 
unable  to  work.  He  was  led  to  believe  that  feigning  was 
very  frequent,  and  he  stated  that  all  the  nervous  symptoms 
resulting  from  railway  accidents  were  either  simulated  or 
else  due  to  organic  injury  of  the  nervous  system. 

The  opinions  as  to  the  extent  of  simulation  have  varied  a 
great  deal  in  Germanv,  where  the  subject  has  received  the 
most  thorough  scientific  attention.  Hoffman  at  one  time 
24 


358 


MALINGERING. 


reported  simulation  in  thirty-three  per  cent  of  his  cases. 
From  several  of  the  alleged  patients  he  obtained  confessions. 
One  man  had  been  coached  by  a  physician  for  the  simulation 
of  epilepsy  ;  another  for  the  pretense  of  anaesthesia.  Seelig- 
miiller  found  simulation  in  twenty-five  per  cent  of  cases; 
Oppenheim  in  four  per  cent.  Shultze  regarded  it  as  fre- 
quent. In  this  country  absolute  simulation  is  generally  con- 
sidered as  unusual.  Knapp,  Dana,  Putnam,  and  others  agree 
in  believing  that  few  persons  could  carry  out,  under  severe 
investigation,  a  system  of  successful  feigning.  Judd  and 
Walton,  on  the  other  hand,  think  the  percentage  of  simula- 
tion is  riot  small.  However,  as  Seguin  says,  in  this  country 
"  claimants  are  very  rarely  subjected  to  scientific  watching 
and  to  repeated  examinations ;  the  physician  or  expert  is 
expected  to  deliver  an  opinion  after  one  or  two  interviews 
with  the  patient,  so  that  the  chances  of  detecting  simulation, 
are  much  reduced." 

But  although  simulation  is  probably  not  very  common,, 
it  is  sufficiently  frequent  for  it  to  be  an  important  factor  in 
the  consideration  of  accident  cases.  "  '  Drag  your  leg,  you 
fool!  don't  you  see  the  doctor  coming?'  was  called  out  by 
a  workman  to  his  fellow  who  had  been  in  an  accident,  and 
heard  by  the  doctor  as  he  was  crossing  the  yard  to  see  him."^ 
(Page.)  Godkin  tells  an  amusing  story  of  a  plaintiff  who- 
testified  "  that  his  right  arm  had  been  so  injured  that  he  was- 
unable  to  raise  it  any  longer  to  a  horizontal  position.  Upon 
cross-examination  the  defendant's  counsel  asked  him  to  indi- 
cate how  high  he  could  now  raise  his  arm.  '  Only  so  high,' 
replied  the  witness,  lifting  his  arm  with  apparent  difficulty  a 
few  inches  from  his  side.  '  And  how  high  could  you  raise 
it  before  this  unfortunate  occurrence?'  asked  the  lawyer 
suddenly.  '  So  high,'  replied  the  witness,  raising  the  same 
injured  arm  above  his  head  with  ease." 

Not  so  very  long  ago  a  man  brought  a  claim  against  a 
Western  railway  for  injury  to  the  spinal  cord,  which  was 


SIMULATION. 


359 


the  alleged  result  of  a  collision.  The  patient  was  apparently 
paralyzed  in  both  legs,  and  for  two  years  was  never  seen  to 
walk  without  crutches.  One  day  at  the  end  of  this  time, 
while  sitting  with  the  claim  agent  in  the  office  of  the  corpo- 
ration, a  settlement  was  agreed  upon,  and  the  man  signed 
the  release  and  received  his  check.  He  arose  briskly  from 
the  chair  and  commenced  to  walk  rapidly  out  of  the  office. 
"  Hullo !  "  said  the  claim  agent,  "  have  you  not  forgotten 
something?"  The  satisfied  claimant  could  not  repress  a 
blush  at  seeing  that  he  had  left  his  crutches  standing  idly  in 
the  corner. 

That  simulation  may  come  to  be  a  systematized  occupa- 
tion and  a  means  of  livelihood  is  well  shown  by  the  Freeman 
family.  In  an  interesting  and  cleverly  written  pamphlet 
entitled  Paralysis  as  a  Fine  Art,  published  in  1895  by  the 
Association  of  Railway  Claim  Agents,  some  of  the  adven- 
tures of  the  Freemans  are  described.  The  family  consisted 
of  a  father,  mother,  and  eight  children,  English  (or  Polish) 
Jews,  all  of  unsavory  reputation  (Fig.  55).  There  is  no  defi- 
nite information  concerning  the  male  members  ;  but  the 
mother,  Mary  Freeman,  and  the  two  daughters,  Jennie  and 
Fannie,  between  January,  1893,  and  December,  1894,  entered 
no  fewer  than  nine  claims  for  damages  against  railway  com- 
panies. That  the  claim  was  fraudulent  and  the  pretenses 
false  in  their  last  attempt  each  and  all  swore  before  a  notary 
in  Chicago  at  the  time  of  their  final  exposure.  There  is  con- 
vincing proof,  also,  that  all  the  claims  that  they  ever  made 
were  fraudulent.  It  may  be  well  to  briefly  outline  how 
these  frauds  were  committed  : 

Mary  Freeman,  the  mother,  was  forty-three  years  of  age,  slov- 
enly in  appearance  and  dress.  "She  was  dirty  and  infested  with 
vermin."  Hers  was  the  ruHng  spirit  of  the  family,  and  she  directed 
the  operation  of  all  the  frauds.  She  had  been  several  times  ar- 
rested for  theft. 

On  September  11,  1894,  she  made  claim  on  the  Chicago  City 


36o 


MALINGERING. 


Railroad  Company  for  injuries  caused  to   her  riglit  arm  by  the 
sudden  starting  of  a  car.     She  received  a  hundred  dollars. 

Jennie  Freeman,  the  eldest  daughter,  was  between  eighteen 
and  twenty-two  years  of  age.  Her  morality  was  questionable. 
She  was  usually 
with  some  physi- 
She  had  been  ar- 
Her  appearance 
pleasing  and  gen- 

On  January  9, 
claim  on  the  Chi- 
road  Company 
ceived  in  a  colli- 
cable  cars.  "  She 
ralysis  from  the 
loss  of  sensation, 
of  the  bowels  and 
and  pretended 
cripple  and  ruined  Jennie  Freeman. 


on  good  terms 
cian  or  attorney, 
rested  for  theft, 
and  manner  were 
tie. 

1893,  she  made 
cago  City  Rail- 
for  injuries  re- 
sion  between  two 
alleged  total  pa- 
thighs  downward, 
want  of  control 
urinary  organs, 
that  she  was  a 
for     life."       The 


Esther  Freeman.  Fannie  Freeman. 

Fig.  55. — Some  members  of  the  Freeman  family. 

company's  physician  "  thought  the  girl  was  shamming,  although 
the  symptoms  were  so  closely  simulated  that  it  was  apparently  a 
real  case  of  paralysis."  The  company  gave  her  five  hundred  dol- 
lars, and  Miss  Jennie  is  said  to  have  recovered  a  few  days  after 
the  damages  were  paid. 


SIMULATION.  361 

If  this  paraplegia  were  genuine,  it  must  have  followed  a  course 
of  unusual  benignity,  for  on  October  5,  1893,  the  patient  made 
claim  on  the  Manhattan  Elevated  Railroad  Company,  of  New 
York,  for  injuries  received  by  falling  against  the  car  door  of  a 
Second  Avenue  train  while  it  was  rounding  the  curve  at  Twenty- 
third  Street.  Settlement  of  one  hundred  dollars  to  her  physician 
and  one  hundred  and  twenty-five  to  Jennie  Freeman. 

On  May  16,  1894,  claim  on  the  Boston  and  Maine  Railroad  of 
having  been  injured  by  slipping  on  a  banana  peel  when  stepping 
out  of  a  car  at  the  Prospect  Hill  Station.  The, banana  peel  was 
produced  in  evidence.  Jennie  Freeman  received  one  hundred  and 
twenty-five  dollars  in  respect  of  these  injuries,  though  the  claim 
agent  suspected  fraud.  She  was  next  heard  of  in  Chicago,  where, 
on  June  28,  1894,  she  brought  claim  on  the  Illinois  Central  Rail- 
road Company  for  injury  received  by  being  thrown  against  the 
back  of  a  seat  through  the  sudden  stopping  of  a  train.  "  She 
alleged  total  insensibility  of  the  lower  portion  of  the  body,  prac- 
tically amounting  to  paralysis.  Had  a  sore  on  her  backbone, 
immediately  above  the  top  of  the  corsets.  Alleged  an  inability  to 
control  the  function  of  the  bowels,  etc.  The  examining  physician 
made  every  possible  test,  but  she  seemed  totally  insensible  to  all 
pain.     The  claimant  was  settled  with  for  two  hundred  dollars." 

On  September  10,  1894,  Jennie  Freeman  alleged  to  have  fallen 
from  her  seat  while  roundmg  a  curve  on  one  of  the  lines  of  the 
West  Chicago  Street  Railroad.  She  represented  to  the  company 
through  her  mother  that  she  was  paralyzed.  Fraud  discovered 
by  claim  agent,  who,  by  an  unexpected  visit,  discovered  the 
alleged  paralytic  sweeping  her  room. 

Fannie  Freeman,  younger  than  Jennie,  was  untidy  in  her  dress, 
quiet,  and  had  little  to  say.     She  had  been  arrested  for  theft. 

On  April  20,  1894,  she  claimed  to  have  been  injured  by  slipping 
on  a  banana  peel  on  the  West  End  Street  Railroad  Company's 
car  in  Boston.  She  complained  of  paralysis  of  motion  and  sensa- 
tion from  the  waist  downward,  and  an  inability  to  control  bladder 
or  rectum.  Over  the  lower  thoracic  vertebrae  there  were  traces 
in  two  places  where  the  skin  had  been  abraded.  The  company's 
physician  says,  in  his  report :  ''  Tenderness  to  pressure  and  per- 
cussion over  the  lumbar  and  dorsal  vertebrae.  Can't  stand,  walk, 
or  sit  unless  completely  supported,  and  then  can  only  be  held  in 
the  half-sitting  and  half-reclining  posture,  all  the  time  evidencing 
great  agony.  When  I  stuck  pins  into  her  feet  and  legs,  and 
touched  them  with  my  hands,  she  declared  she  could  not  feel  any 


362 


MALINGERING. 


sensation,  and  1  couldn't  surprise  her  into  any  painful  expression." 
The  prognosis  was  given  as  unfavorable,  and  Fannie  Freeman  was 
paid  three  hundred  and  twenty-five  [or  four  hundred  and  twenty- 
five]  dollars. 

On  June  6,  1894,  Fannie  Freeman,  under  an  assumed  name, 
made  claim  on  the  New  York,  New  Haven,  and  Hartford  Railroad 
Company  at  Boston.  This  case  was  an  identical  reproduction  of 
the  preceding,  even  to  the  patient's  maintaining  that  it  was  "  her 
first  accident."  But  she  was  unfortunate  in  being  visited  by  the 
same  examiner  who  had  seen  her  a  month  previously  for  the 
West  End  Street  Railroad  Company.  For  the  physician  this 
time  recognized  the  fraud,  which  he  had  failed  to  do  in  the  first 
instance. 

On  December  24,  1894,  ]\Iary  Freeman  claimed  to  the  general 
superintendent  of  the  Chicago,  Rock  Island,  and  Pacific  Railroad 
Company,  Chicago,  that  her  daughter  Fannie  had  been  injured  by 
falling  on  the  back  in  a  car  of  the  company.  She  alleged  that  her 
daughter  was  paralyzed  from  the  waist  down,  and  had  lost  all 
sensation  in  the  legs ;  that  there  was  no  power  over  the  rectum  or 
bladder,  and  that  the  young  girl  was  ruined  for  life.  There  were 
so  many  suspicious  circumstances  about  the  case  that  the  family 
were  watched.  Before  the  expected  visit  of  the  company's  doc- 
tors the  alleged  cripple  was  seen,  from  a  hole  through  the  floor  of 
a  room  above  hers,  to  get  nimbly  out  of  bed  and  put  her  feet  in  a 
tub  of  iced  water,  in  order  that  they  might  feel  cold  and  lifeless 
to  the  examiners. 

Some  of  the  results  of  the  medical  examination,  as  embodied 
in  the  surgeon's  report,  are  as  follows : 

"  Pulse  at  first  104,  but  it  changed  so  that  at  the  last  of  the 
examination  it  was  132.  Her  back  was  marked  by  a  slight  spot 
about  the  top  of  the  sacrum,  entirely  superficial  and  movable  over 
the  underlying  tissues,  which  may  have  been  produced  by  some 
injury,  or  by  the  abrasion  of  some  part  of  her  clothing.  Sensation 
existed  about  halfway  down  the  thighs,  but  below  this  point  it  was 
alleged  to  be  absent.  There  were  no  evidences  observed  of  in- 
continence of  urine  or  fseces,  and  no  girdle  sensation  was  com- 
plained of.  An  unexpected  test  of  raising  the  foot  in  the  air 
caused  it  to  stop  there,  though  tests  of  physical  endurance  were 
applied  and  successfully  withstood." 

The  doctors  were  satisfied  of  the  fraud,  and  reported  that  there 
were  no  objective  evidences  of  the  conditions  complained  of. 

The  following  day  the  three  women  were  arrested.      Fannie 


SIMULATION.  26-, 

Freeman,  "the  paralyzed   lady,  jumped   out  of  bed,  cursed,  and 
inarched  around  the  room  with  a  tramp  like  a  grenadier." 

The  Freeman  cases  have  been  quoted  in  some  detail 
because  there  seems  little  reason  to  doubt  that  all  the  claims 
were  absolutely  fraudulent,  and  that  the  symptoms  in  each 
case  were  entirely  fictitious. 

The  cases  in  which  there  is  a  detailed  report  of  the  med- 
ical examination  show  how  far  and  in  what  way  the  symp- 
toms of  nervous  disease  may  be  simulated.  Certain  of  the 
symptoms  of  the  Freemans  will  be  referred  to  again. 

Difficulties. — In  accident  cases  simulation  is  attempted 
with  the  sole  object  of  gain.  Reference  has  already  been 
made  to  the  temptations  which  lead  to  this  particular  form 
of  dishonesty.  Yet,  while  the  bait  is  alluring,  the  person 
who  makes  a  claim  for  personal  injuries,  when  in  reality  he 
has  not  been  injured  at  all,  sets  himself  a  task  of  no  little 
difficulty.  In  the  first  place,  he  must  give  some  account  of 
himself  and  of  his  social  relations.  He  may  be  able  to  satis- 
factorily conceal  his  past  if  he  has  anything  to  conceal.  Of 
course,  a  notorious  rogue  would  probably  be  detected  at 
once  ;  and  the  appearance  and  methods  of  an  impostor  who 
has  been  caught  by  any  large  corporation  might  be  recog- 
nized when  he  brings  claim  against  some  other  company. 
Fannie  Freeman  was  on  one  occasion  detected  in  Boston 
because  she  was  examined  by  the  same  ph3'sician  who  had 
seen  her  a  month  previously  for  another  company.  Claim 
■agents  also  exchange  for  mutual  benefit  any^  information 
which  they  may  gather  in  regard  to  suspicious  characters. 
The  system  with  them  is  not  so  highly  elaborated  as  is  the 
system  of  exchange  by  life-insurance  companies  of  the 
names  of  rejected  candidates,  but  it  is  usually  sufficient,  to 
brand  a  man  who  has  been  detected  shamming  several 
times. 

The  past  record,  however,  the  successful  simulator  may 


3^4 


MALINGERING. 


be  able  to  conceal,  if  concealment  is  necessary.  It  is  more 
difficult  for  him  to  prove  himself  of  a  character  and  position, 
the  possessors  of  which  do  not  ordinarily  resort  to  flagrant 
and  absolute  imposture.  In  this  respect  the  absolute  simula- 
tor is  very  different  from  the  person  who  exaggerates  actual 
though  slight  injuries.  Symptoms  may  be,  and  occasionally 
are,  dishonestly  magnified  by  persons  whose  reputations  for 
integrity  have  escaped  suspicion,  and  who  are  regarded  as 
estimable  members  of  society.  But  such  persons  are  rarely 
absolute  simulators.  The  simulator  crosses  the  border  land 
of  deceit  and  takes  his  place  among  criminals.  If  he  can  not 
prove  himself  as  following  some  respectable  calling,  the  suc- 
cess of  his  venture  is  hazarded.  Claim  agents  show  an  in- 
clination to  know  as  much  as  possible  about  personal  habits 
and  modes  of  life  of  the  claimant  before  they  consider  ad- 
justment, and  the  impossibility  of  furnishing  satisfactory 
details  of  this  character  undoubtedly  deters  many  who 
otherwise  would  cheerfully  undertake  to  defraud  by  feign- 
ing disease. 

Even  when  the  simulator  is  able  to  furnish  satisfactory 
proof  of  his  honesty  and  respectability  there  still  remain  for 
him  serious  difificulties.  To  closely  imitate  nervous  disease 
requires  no  mean  order  of  intellect.  A  clever  simulator 
must  have  quickness  in  adapting  himself  to  new  situations^ 
a  plausible  and  ingenuous  manner,  the  power  of  close  atten- 
tion, a  good  memory,  and  some  knowledge  of  the  symptoms 
of  disease  of  the  nervous  system.  These  are  mental  qualifi- 
cations all  of  which  are  rarely  present  in  the  individuals 
who  resort  to  the  feigning  of  disease  for  financial  purposes  ; 
yet  all  of  them  must  be  present  if  a  physician  who  is  reason- 
ably skillful  and  who  is  on  the  lookout  for  shams  is  to  be 
made  to  believe  that  the  symptoms  are  genuine  when  in 
reality  they  are  entirely  assumed. 

The  simulator  must  hold  himself  ready  for  examination 
at  any  time.     Examinations  made  at  the  most  unexpected 


SIMULATION. 


365 


hours  or  in  rapid  succession  should  find  him  always  prepared 
to  reproduce  an  essentially  unvarying  chain  of  symptoms. 
He  may  be  successively  submitted  to  the  observation  of 
physicians  of  different  ability  who  make  examinations  of 
different  characters  in  diverse  ways.  To  deceive  them  all, 
the  simulator  must  have  his  wits  about  him.  The  general 
appearance  and  manner,  which  are  among  the  most  reliable 
signs  for  medical  diagnosis,  must  to  a  certain  extent  cor- 
respond with  the  bearing  of  persons  who  really  suffer  from 
the  symptoms  he  is  trying  to  imitate.  These  evidences  are 
the  outward  expressions  of  the  morbid  agencies  which  are 
at  work ;  they  are  difficult  to  describe  and  still  more  diffi- 
cult to  counterfeit.  A  knowledge  of  their  significance  and 
characteristics  in  disease  is  only  acquired  by  long  experience 
in  general  medical  practice,  a  fact  which  constitutes  perhaps 
the  most  serious  stumbling  block  to  the  simulator.  Even  if 
he  had  the  necessary  knowledge  of  the  general  appearances 
in  nervous  diseases,  they  are  symptoms  almost  impossible  to 
successfully  imitate.  They  reveal  the  condition  of  the  whole 
organism  and  are  largely  beyond  the  power  of  voluntary 
control.  When  the  simulator  tries  to  copy  them  he  over- 
does it.  His  manner  is  exaggerated  and  theatrical  ;  his 
symptoms  are  severer  than  real  symptoms  usually  are  ;  his  • 
prospects  are  ruined.  Yet  with  it  all  are  wanting  the  ob- 
jective evidences  which  almost  invariably  accompany  such 
severe  symptoms.  The  eye  is  bright,  and  the  face,  seen  in 
repose,  belies  the  assertion  of  constant  physical  and  mental 
torture.  It  is  the  exaggerated  character  of  the  story  that 
often  at  once  excites  the  physician's  suspicion  and  leads  him 
to  apply  searching  tests  which  result  in  exposure. 

Without  remarkable  powers  of  attention  the  simulator 
can  not  hope  to  meet  with  much  success.  He'  must  be  al- 
ways ready  to  be  examined  and  constantly  on  the  alert 
even  when  he  does  not  suspect  himself  of  being  observed. 
When  under  direct  examination  or  observation  he  must  be 


366 


MALINGERING. 


€ver  on  his  guard  not  to  be  caught  b}^  tricks  nor  to  be  be- 
trayed by  his  own  emotions.  Page  tells  of  "  a  man  who 
based  a  large  demand  for  compensation  from  a  raihva}-  com- 
pany on  stiffness  of  the  elbow  and  inability  to  move  the 
arm,  the  result  of  a  collision.  A  verdict  incommensurate 
with  his  expectations  having  been  recorded,  he  threw  up 
his  arms  and  exclaimed,  '  My  God  !  I'm  a  ruined  man.'  " 

To  sham  any  form  of  disease  requires  that  several  symp, 
toms  must  be  counterfeited  at  the  same  time.  To  imitate 
any  one  objective  symptom  successfully  for  the  length  of 
time  usuall}"  taken  for  medical  examination  requires  a  very 
close  attention  ;  to  simulate  several  simultaneously  is  for  the 
majority  of  persons  impossible.  To  keep  constantly  before 
the  mind  that  the  legs  must  not  move,  that  pin  pricks  must 
not  hurt,  and  that  movements  of  the  back  are  painful,  is  an 
intellectual  exercise  of  considerable  activity.  If  these  symp- 
toms do  not  really  exist,  the  attention,  while  one  of  them  is 
being  examined,  is  usually  concentrated  on  it  at  the  expense 
of  the  others.  As  a  result,  alleged  paralyzed  legs  may  be 
seen  to  move,  movements  of  the  back  may  no  longer  cause 
suffering  to  the  subject,  or  he,  may  be  startled  into  involun- 
tary expressions  of  pain  when  pricked  in  areas  said  to  be 
anaesthetic.  A  long  and  thorough  examination,  especially  if 
the  examiner  be  suspicious  of  fraud,  will  usually  disclose 
some  or  all  of  the  symptoms  to  be  false.  Even  when  the 
simulator  is  entirely  conversant  with  the  character  of  the 
disturbances  he  is  shamming  he  is  rarely  able  to  keep  himself 
from  being  confused  by  their  examination  in  rapid  succes- 
sion. Fannie  Freeman,  who  was  undoubtedly,  by  experience 
and  by  teaching,  thoroughly  conversant  with  the  symptoms 
of  paraplegia,  forgot  to  let  her  leg  drop  when  it  was  lifted 
up  by  the  examiner.  Instead  of  falling  lifelessl}^  to  the  bed, 
as  it  should  have  done,  it  was  held  in  the  air,  and,  by  suc- 
cessfully resisting  the  efforts  of  the  doctors  to  push  it  down, 
showed  a  high  degree  of  muscular  strength. 


SIMULATION.  367 

A  qualification  closely  allied  to  power  of  attention  is  a 
good  memory.  It  is  very  essential,  if  a  story  is  to  be  be- 
lieved, that  when  retold  it  remains  essentially,  though  not 
minutely  the  same.  Many  claimants  excite  suspicion  by  the 
variations  and  inconsistencies  which  appear  when  they  re- 
late the  details  of  the  accident  to  different  persons.  Genuine 
symptoms  have  a  certain  permanency.  A  clumsy  simulator 
will  often  forget,  when  talking  about  his  case  to  one  ex- 
aminer, just  what  he  has  complained  of  to  the  claim  agent 
or  to  the  physician  whom  he  had  seen  before.  On  the  other 
hand,  it  is  not  always  just  to  infer,  because  a  history  of  in- 
jury or  symptoms  is  indefinite  or  contradictory,  that  the 
claimant  is  an  impostor.  Both  the  memory  and  attention 
are  impaired  to  a  certain  extent  in  neurasthenia,  and  still 
more  so  in  hysteria ;  but  all  such  inconsistencies  will  cause 
a  claimant  to  be  regarded  with  suspicion  until  it  can  be 
proved  with  a  remarkable  degree  of  certainty  that  they  are 
not  the  results  of  clumsy  and  voluntary  attempts  at  de- 
ception. 

Knapp  believes  that  simulation  must  be  rare,  because  the 
larger  number  of  persons  who,  would  be  willing  to  fraudu- 
lently feign  disease  are  unable  to  obtain  a  sufficient  knowl- 
edge of  symptoms  to  successfully  imitate  them  ;  that  simu- 
lators are  of  a  class  rarely  able  to  refer  to  medical  books, 
and  that  physicians  who  might  be  able  to  give  instruction 
in  this  kind  of  fraud  could  not  be  persuaded  to  do  so.  It 
seems  to  me  that  lack  of  medical  knowledge,  in  accident 
cases  at  least,  is  one  of  the  minor  difSculties  against  which 
the  simulator  has  to  contend.  When  a  large  claim  is  made 
and  the  company  decides  to  contest  it,  the  chances  of  suc- 
cessful simulation  are  always  small.  The  simulator  fails 
then,  both  because  his  motives  are  very  thoroughly  investi- 
gated and  because  he  is  subjected  to  a  series  of  rigid  exami- 
nations. But  in  by  far  the  larger  number  of  instances  the 
case  does  not  come  to  trial,  because  the  claim  made  is  gen- 


368  MALINGERING. 

erally  small,  and  the  companies  find  it  cheaper  to  settle  it 
than  to  go  to  the  expense  of  trial  and  expert  opinion.  In 
this  way  a  simulator,  without  being  particularly  expert,  may 
escape  exposure,  although  both  claim  agent  and  physician 
suspect  him  of  being  a  swindler. 

The  form  of  disease  most  commonly  simulated  is  neu- 
rasthenia, for  which  no  special  knowledge  is  necessary. 
The  general  symptoms  of  "  railway  spine  "  are  familiar  to 
most  physicians,  even  though  they  be  unacquainted  with 
general  nervous  diseases.  Physicians  can  very  easily  simu- 
late railway  spine  or  teach  how  it  should  be  simulated,  and 
experience  shows  that  they  sometimes  do  so.  The  condi- 
tion can  also  be  feigned  with  moderate  accuracy  by  persons 
who  know  nothing  of  general  medicine.  There  are  no 
positive  objective  symptoms  by  which  the  fraud  can  be 
discovered,  and  there  are  a  great  many  persons  who,  with- 
out any  medical  degree,  have  acquired  sufficient  familiarity 
with  various  forms  of  disease  to  give  a  fairly  good  reproduc- 
tion of  the  picture  of  neurasthenia.  Inmates,  attendants,  and 
hangers-on  of  various  hospitals  and  public  institutions  gen- 
erally become,  through  long  experience,  well  acquainted  with 
the  different  forms  of  human  suffering.  Page  remarks  upon 
the  knowledge  possessed  by  persons  in  the  humbler  walks 
of  life,  regarding  the  history  and  symptoms  of  the  kind  of 
injury  which  is  popularly  supposed  to  be  inevitable  to  a  rail- 
way collision.  Knowledge  of  the  symptoms  of  neurasthenia 
may  be  easily  acquired.  If  the  simulator  can  not  learn  them 
himself,  there  is  little  reason  to  suppose  that  he  would  have 
any  serious  difficulty  in  finding  a  physician  ready  and  able 
to  instruct  him.  Knowledge  of  the  symptoms  of  organic 
nervous  disease  is  more  difficult  to  obtain,  and  most  physi- 
cians who  would  impart  it  for  fraudulent  purposes  do  not 
themselves  know  very  much  about  them.  But  simulation 
of  organic  nervous  disease  can  onl}'  be  successful  when  the 
examiner  is  himself  careless  or  unfamiliar  with  the  symp- 


SIMULATION. 


369 


toms  and  the  means  of  demonstrating  them,  for  organic 
nervous  disease  can  not  be  feigned  with  any  degree  of  re- 
semblance. With  assumed  symptoms  indicative  of  organic 
disease,  if  the  simulator  passes  undetected  it  is  less  of  a  testi- 
monial to  his  knowledge,  than  it  is  a  proof  that  the  examin- 
ing physician  has  been  superficial,  careless,  or  ignorant. 

Detection  of  Simulation. — The  physician's  part  in  the 
detection  of  simulation  is  to  show  that  the  clinical  picture  is 
not  produced,  a  task  that  is  rendered  easy  by  an  appreciation 
of  the  various  factors  which  of  themselves  make  the  simula- 
tor's part  so  difficult.  While  some  simulators  are  so  clumsy 
that  they  are  immediately  turned  away  from  the  claim 
agent's  door,  well-trained  impostors  like  the  Freemans  merit 
the  best  skill  of  the  medical  man.  For  the  exposure  of  such 
experienced  swindlers  as  they  were,  the  physician  must  not 
only  be  on  his  guard,  but  he  must  constantly  keep  on  the 
defensive  the  person  he  is  examining.  B}'  bearing  in  mind 
the  disadvantages  under  which  the  simulator  is  placed  the 
examiner  can,  in  many  ways,  render  them  still  more  em- 
barrassing. The  detection  of  skillful  simulation  of  any  one 
symptom  depends  upon  diverting  the  simulator's  atten- 
tion. He  must  be  taken  off  his  guard.  When  he  does  not 
know  that  he  is  being  \vatched,  the  phj^sician  may  find  that 
the  facial  expression  undergoes  a  marked  change.  Com- 
plaints of  pain  may  be  forgotten  if  he  can  be  made  to  talk 
of  something  not  directly  relating  to  the  accident.  If  the 
examination  is  sufficiently  long,  it  is  generally  found  that 
there  are  periods  during  which  the  expressions  of  suffering 
momentarily  cease.  These  lapses  may  be  short,  and  the 
simulator  may  soon  collect  himself  again.  But  a  momentary 
forgetfulness  of  this  character  should  at  once  excite  the  phy- 
sician's suspicion.  It  is  by  attracting  the  patient's  attention 
away  from  the  symptom,  the  true  nature  of  which  the  phy- 
sician desires  to  assure  himself,  that  the  fraud  frequently 
becomes  apparent.     It  is  very  hard  to  think  for  any  length 


370 


MALINGERING. 


of  time  on  two  things  at  once,  and  if  the  examiner  is  in  real- 
ity examining  for  one  symptom  while  he  appears  to  be  test- 
ing another,  he  may  often  be  able  to  prove  that  one  of  the 
symptoms  exists  only  when  the  person  under  examination 
has  his  attention  fixed  upon  it. 

Detection  of  the  simulation  of  those  disorders  which  may 
result  from  accidents  is  in  most  cases  possible.  Clinical  pos- 
sibilities are  limited,  and  when  a  man  says  he  is  suffering 
from  the  effects  of  an  accident,  the  question  immediately 
arises.  What  is  the  pathological  condition  to  which  the 
symptoms  are  due?  By  eliminating  disorders  with  which 
the  symptoms  do  not  agree  at  all,  the  physician  who  is 
familiar  with  the  various  morbid  conditions  which  cause  dis- 
turbance of  nervous  function  can  reduce  the  possibilities  in 
any  case  to  the  one  or  two  conditions  with  which  the  symp- 
toms agree  most  closely.  It  then  remains  for  him  to  deter- 
mine if  the  resemblance  to  either  or  both  of  these  conditions 
is  sufficiently  close  to  justify  the  symptoms  being  regarded 
as  genuine  and  not  feigned.  For  example,  an  allegation  that 
the  arm  is  injured  is  not  enough.  It  should  be  shown  how 
it  is  injured,  and  if  careful  examination  shows  that  it  is  sur- 
gically intact,  and  that  the  symptoms  are  at  variance  with 
those  of  any  known  variety  of  nerv^ous  condition,  it  is  entirely 
justifiable  to  infer  that  the  arm  is  not  injured  at  all.  Page 
reports  a  case  in  which  the  dribbling  of  urine  caused  by  a 
large  prostate  was  alleged  to  be  due  to  injury  to  the  spinal 
cord.  The  man  was  not  paralyzed,  and  he  was  at  once 
recognized  as  an  impostor,  because  any  injury  to  the  spinal 
cord  which  could  cause  weakness  of  the  vesical  sphincter 
would  cause  paralysis  or  some  other  symptom  of  spinal-cord 
injury. 

Similarly,  Fannie  Freeman,  in  her  last  attempt,  might 
have  been  detected  at  once,  from  the  fact  that  she  failed  to 
make  her  paralysis  agree  with  any  known  form  of  paraplegia  ; 
for,  with  alleged  complete  loss  of  power  of  the  lower  limbs 


SIMULATION, 


371 


and  of  the  bladder  and  rectum,  the  feigned  anaesthesia  only 
reached  to  the  middle  of  the  thighs.  If  the  paralysis  had 
been  due  to  injury  to  the  spinal  cord,  the  anaesthesia  would 
have  had  a  very  different  distribution.  If  the  whole  condi- 
tion had  been  hysterical,  the  sphincters  would  have  remained 
unimpaired. 

The  choice  of  diseases  for  simulation  is  restricted,  inas- 
much as  the  variety  of  nervous  disorders  which  may  result 
from  injury  is  not  large.  Acute  organic  injury  to  the  brain,, 
spinal  cord,  or  peripheral  nerves  causes  symptoms  which  can 
not  be  feigned.  General  paresis,  progressive  muscular  atro- 
phy, and  tabes  can  not  be  copied  with  even  a  shadow  of  re- 
semblance. Feigned  paralysis  agitans  would  quickly  be  pro- 
nounced spurious  by  any  medical  student  who  had  examined 
one  genuine  case  of  that  disease.  Epilepsy  is  rarely  feigned 
in  accident  cases,  and  usually  appears  in  the  form  of  a 
genuine  epileptic  alleging  that  the  disease  was  caused  by 
injury.  If  epilepsy  is  alleged  as  the  result  of  accident,  the 
evidence  of  non-medical  witnesses  of  the  fit  should  be  re- 
garded as  insufficient  proof. 

Neurasthenic  disturbances  are  the  ones  most  frequently 
complained  of  by  simulators,  who  are  quick  to  take  advan- 
tage of  a  condition  which  is  practically  devoid  of  objective 
symptoms.  It  is  in  these  cases  especially  that,  as  Page  says, 
"  it  is  only  by  a  consideration  of  every  feature  and  aspect  of 
the  case — clinical,  pathological,  social,  and  moral — that  you 
can.  rightfully  estimate  the  kind  of  exaggeration  or  malin- 
gering with  which  you  have  to  do."  The  physician  may 
believe  that  a  case  of  neurasthenia  is  absolutely  feigned  ; 
but  unless  he  has  some  definite  proof  upon  which  to  base 
his  opinion  he  is  not  justified  in  calling  the  man  a  swindler. 
If  a  claimant  restricts  himself  to  assertions  of  pain  in  the 
back,  loss  of  energy,  inability  to  do  his  work,  and  similar 
complaints  of  purely  subjective  character,  the  physician 
may  be  sure  that  the  symptoms  are  exaggerated,  but  he  cau 


372 


MALINGERING. 


not  show  that  they  are  false.     The  truth  in  regard  to  claims 
which  are  based  upon  symptoms  of  such  a  character  must 
be  determined  by  general  considerations  and  by  information 
gained  from  sources  other  than  the  medical  examiner. 
Hysteria  is  probably  never  simulated  in  America. 

A  claim  agent,  in  telling  me  of  many  cases  from  his  experience 
in  which  the  symptoms  had  speedily  disappeared  after  settlement, 
said  that  there  was  one  case  he  had  never  been  able  to  understand. 
A  man  had  received  a  slight  injury  in  a  collision,  as  a  result  of 
which  he  alleged  that  his  legs  were  paralyzed.  In  spite  of  many 
circumstances  which  appeared  suspicious,  the  claimant  was  com- 
pensated. But  the  injured  man,  instead  of  getting  well,  remained 
a  paralytic,  and  it  became  generally  believed  that  his  spinal  cord 
really  had  been  injured.  Two  years  after  the  damages  were  paid 
he  suddenly  regained  full  power  of  the  legs.  The  fact  that  this 
case  was  misunderstood  is  in  accord  with  the  common  opinion, 
both  lay.  and  medical,  held  in  America  in  regard  to  hysteria. 

It  is  not  generally  appreciated  that  hysteria  is  a  disease 
and  not  premeditated  swindling.  Until  the  subjective  real- 
ity of  hysterical  symptoms  becomes  more  generally  believed 
in,  the  disease  can  not  be  popular  with  simulators.  To  feign 
a  disease  which  is  itself  regarded  as  fraud  would  be  worse 
than  useless.  But  the  failure  to  recognize  that  symptoms 
are  hysterical  and  not  voluntarily  created  may  cause  much 
injustice  to  the  hysterical  patient.  He  may  be  immediately 
branded  as  an  impostor  the  moment  the  objective  symptoms 
are  shown  not  to  be  organic.  There  is  more  probability  of 
a  hysterical  person  being  classed  as  a  simulator  than  of  a 
simulator  attempting  to  feign  hysteria.  The  diagnosis  be- 
tween hysteria  and  simulation,  however,  should  not  be  diffi- 
cult to  any  one  who  is  familiar  with  hysterical  symptoms. 
Hysteria  is  the  cleverest  simulator  of  all,  and  is  adroit  and 
consistent  when  the  simulator  is  clumsy  and  confused.  The 
hysteric  copies,  while  the  simulator  caricatures.  Hysteria 
causes  its  victim  to  involuntarily  mimic  organic  disease 
much  more  closely   than   organic    disease   can   be    imitated 


SIMULATION   OF    INDIVIDUAL   SYMPTOMS.  373 

voluntarily.  But  even  the  mimicry  of  hysteria  is  not  per- 
fect, and  by  the  irregularity  and  association  of  its  symptoms 
it  can  readily  be  differentiated  from  organic  disease. 

The  forms  of  disease  which  have  been  described  as 
unclassified  are  accompanied  by  symptoms  too  serious  to 
permit  them  to  be  misinterpreted  or  imitated. 

An  individual  or  a  corporation  which  is  being  sued  for 
damages  for  personal  injuries  should  be  entitled  to  ascertain 
the  character  and  extent  of  the  injury  for  which  he  is  held 
responsible.  Viewed  from  a  purely  commercial  standpoint, 
he  has  a  right  to  know  what  he  is  paying  for,  or,  in  other 
words,  to  insist  upon  a  definite  diagnosis  before  payment  is 
made.  Such  diagnoses,  if  they  can  not  be  made  at  once, 
usually  become  possible  after  the  observation  of  a  few  days 
or  weeks.  When  the  possibilities  of  exactness  in  diagnosis 
of  disorders  of  the  nervous  system  are  more  generally  recog- 
nized, and  when  "  shattered  nerves,"  and  similar  meaningless 
■designations  come  to  be  regarded  as  insufficient  claims  in 
neofliofence  cases,  the  detection  of  simulation  will  be  rendered 
very  much  easier.  The  simulator  would  then  be  forced  to 
choose  some  definite  condition  to  feign,  and  to  have  all  his 
symptoms  in  accord  with  it. 

The  symptoms  most  difficult  to  simulate,  or  even  to  ex- 
aggerate, are  those  known  as  objective.  They  are  of  suffi- 
cient importance,  however,  to  be  considered  in  detail. 

Simulation  of  Individual  Symptoms. 
Motion. — The  most  difficult  objective  symptom  to  coun- 
terfeit is  the  loss  of  voluntary  motor  power.  If  the  simulator 
decides  to  enlarge  upon  the  simple  complaint  of  pain  in  the 
back  and  general  nervousness,  he  is  very  apt  to  be  led  away 
by  the  attractive  picture  of  paralysis.  By  refusing  to  move 
his  limbs,  or  by  giving  them  the  appearance  of  lifelessness 
when  they  are  handled  by  the  examiner,  it  seems  to  him 
comparatively  easy  to  substantiate  the  statement  that  certain 
25 


374 


MALINGERING. 


muscles  have  lost  their  power  of  voluntary  movement.  He 
loses  sight  of  the  fact,  however,  that  true  paralysis  has  cer- 
tain signs  which  are  impossible  of  voluntary  imitation,  and 
that  it  is  well-nigh  useless  to  attempt  to  impose  in  this  way 
upon  a  careful  physician  who  is  familiar  with  the  various 
phases  and  causes  of  impairment  or  loss  of  muscular  power. 

There  are  two  reasons  which  seem  to  justify  the  state- 
ment that  true  paralysis  can  not  be  well  feigned.  One  is 
that  the  condition  of  the  muscles  themselves — the  flabbiness, 
softness,  and  lack  of  tone — can  not  be  voluntarily  counter- 
feited with  any  great  degree  of  similarity.  The  other  reason 
is  that  organic  paralysis  does  not  occur  as  an  isolated  symp- 
tom, but  is  invariably  accompanied  by  others  which  are  com- 
pletely beyond  the  control  of  the  will. 

If  paralysis  is  simulated,  when  the  limb  is  lifted  up  and 
suddenly  released  it  may  be  held  a  moment  before  it  is 
dropped  again  ;  or  if  the  examiner  tries  to  move  the  limb, 
his  hand  may  detect  that  there  is  a  moment  in  which  the 
muscles  are  held  stiff,  although  they  relax  again  as  soon  as 
the  subject  discovers  the  object  of  the  test ;  or  the  limb  may 
be  seen  to  move  under  the  influence  of  painful  stimuli,  or 
when  the  person  under  examination  forgets  to  hold  it  mo- 
tionless. 

Paralysis  is  rarely  isolated.  Appearing  acutel}^  it  can 
only  take  place  as  the  result  of  organic  injury  to  the  nerv- 
ous system  or  of  the  fixed  ideas  of  hysteria.  If  the  brain 
is  the  seat  of  a  lesion  there  may  be  a  resulting  hemiplegia 
or  monoplegia,  but  the  paralysis  is  ushered  in  with  con- 
siderable cerebral  disturbance.  Paralysis  due  to  primary 
intracranial  lesions  rarely  occurs  without  unconsciousness 
or  convulsions  or  severe  headaches,  or  some  similar  severe 
cerebral  symptoms.  The  functions  of  the  cranial  nerves  can 
not  be  voluntarily  suppressed.  A  man  may  claim  that  he 
does  not  taste,  see,  or  hear,  statements  which  may  be  difficult 
to  verify  ;  but  he  can  not  voluntarily  cause  permanent  devia- 


SIMULATION   OF   INDIVIDUAL   SYMPTOMS.  375 

tion  of  the  eyes,  such  as  results  from  palsy  of  the  nerves  to 
the  ocular  muscles,  nor  can  he  keep  his  face  drawn  to  one 
side  S'o  that  it  does  not  become  apparent,  during  movements 
of  talking-  or  laughing,  that  the  facial  nerve  is  not  paralyzed. 
Hemiplegia  is  usually  quickly  followed  by  unilateral  changes 
in  reflex  activity  which,  as  we  shall  see,  can  not  be  imitated 
in  a  way  to  deceive  any  one  familiar  with  these  important 
evidences.  The  symptoms  of  hemiplegia,  as  the  result  of 
injur}^  are  too  complex  for  the  average  simulator,  and  are 
pictures  with  which  he  is  usually  unfamiliar.  Any  attempts 
to  copy  them  must  be  unusual,  if  they  are  ever  made. 

Loss  of  power  in  the  legs  seems  to  the  simulator  the 
clinical  type  most  consistent  with  the  general  theory  of  pa- 
ralysis which  follows  accidents.  Injury  to  the  spine  with 
resulting  paralysis  of  the  legs  is  a  comparatively  common 
condition,  and  the  average  simulator  is  rarely  a  sufficiently 
profound  pathologist  to  recognize  the  fact  that  traumatic 
paraplegia  is  most  frequently  the  result  of  fracture  or  dislo- 
cation of  the  vertebrae,  such  as  only  occur  after  very  severe 
accidents.  Furthermore,  organic  injury  to  the  spinal  cord  is 
without  exception  accompanied  by  many  symptoms  which 
do  not  permit  of  voluntary  imitation.  Trophic  disturbances 
are  beyond  the  realm  of  imitative  art ;  by  soaking  the  legs 
in  iced  water  they  may  be  made  to  feel  cold  and  look  blue, 
but  there  is  nothing  but  actual  nerve  injury  which  can  cause 
the  appearance  of  a  beginning  bedsore,  and  the  cleverest 
actor  can  not  make  his  muscles  waste  or  his  nerves  give 
degenerative  electrical  reactions.  In  recent  organic  para- 
plegias there  is  a  softness  and  flabbiness  of  the  muscles 
which  is  characteristic  ;  and  as  the  paralysis  of  some  muscles 
passes  away,  as  it  usually  does  in  time,  they  resume  their 
normal  tonic  action.  But  the  muscles  remaining  paralyzed 
offer  no  resistance  to  their  opponents,  and  contractions 
and  deformities  are  the  results.  Organic  paraplegia  is  usu- 
ally accompanied   with    some  trophic  symptoms,  together 


376 


MALINGERING. 


with  angesthesia  and  changes  in  reflex  activity.  Even  with- 
out the  aid  of  them,  it  is  usually  possible  in  any  case  to 
demonstrate  whether  the  paralysis  is  true  or  feigned.    ■ 

The  simulation  of  organic  monoplegia  is  still  more  diffi- 
cult. It  is  often  alleged  that  the  arm  is  injured,  but  these 
are  cases  which  are  characterized  by  peripheral  rather  than 
central  injuries.  The  neurologist  can  at  once  decide  if  there 
has  been  any  injury  to  peripheral  nerves,  and  a  surgical  ex- 
amination should  quickly  discover  the  integrity  of  the  bones 
and  joints.  In  the  absence  of  any  such  evidences  of  periph- 
eral injury  it  is  justifiable  to  infer  that  the  case  is  feigned 
or  hysterical.  Traumatic  monoplegia  from  any  cause  is 
very  rare,  and  as  a  result  of  spinal  injury  it  is  practically 
unknown,  which  may  be  explained  by  the  fact  that  the 
spinal  localization  for  the  movements  of  any  one  limb  ex- 
tends over  several  segments  of  the  cord.  Any  injury  which 
affects  a  sufficient  number  of  segments  to  cause  a  monople- 
gia will  be  accompanied  by  paralyses  of  other  parts. 

Hysteria  can  imitate  better  than  any  simulator  the  or- 
ganic paralyses  and,  as  has  been  said,  there  is  more  danger 
that  the  involuntary  mimicry  of  hysteria  be  regarded  as  de- 
liberate imposture  than  that  the  impostor  who  feigns  para- 
plegia may  pass  undetected.  The  decision  of  the  question 
between  hysterical  paralysis  and  simulation  may  be  very 
difficult.  If  the  plaintiff's  physician  assert  that  his  client  is 
suffering  from  organic  paralysis,  the  truth  of  the  statement 
may  be  determined  with  certainty.  But  if  the  claim  should 
be  made  (it  rarely  is)  that  the  paralysis  is  functional,  it  may 
be  impossible  to  refute  it  by  objective  signs.  The  character- 
istics of  hysterical  paralysis  have  already  been  described  in 
such  detail  that  it  will  be  sufficient  to  recall  the  fact  that 
they  differ  in  essential  particulars  from  the  paralyses  arising 
from  organic  causes.  But  the  differences  are  very  similar 
to  those  which  exist  between  organic  paralysis  and  feigned 
loss  of  muscular  power.     The  hysteric,  like  the  simulator, 


SIMULATION   OF    INDIVIDUAL   SYMPTOMS. 


377 


suffers  neither  from  bedsores  nor  from  loss  of  sphincter 
control;  he  drags  his  foot  on  the  side  rather  than  at  the 
toe  ;  there  is  no  circumduction  of  the  leg ;  there  are  usually 
no  changes  in  the  reflexes ;  hysterical  symptoms  are  more 
marked  when  the  patient  knows  that  he  is  being  watched. 
In  a  word,  although  hysteria  can  not  imitate  the  motor 
symptoms  which  do  not  permit  of  voluntary  imitation,  there 
are  many  cases  in  which,  from  the  character  of  the  motor 
symptoms  alone,  it  can  not  be  inferred  whether  the  condi- 
tion is  the  result  of  premeditated  deceit  or  of  the  uncon- 
scious mimicry  of  hysteria.  To  decide  this  question  recourse 
must  be  had  to  other  symptoms. 

In  the  larger  number  of  the  cases  of  hysteria  the  asso- 
ciated signs  are  sufficient  to  permit  the  disorder  to  be  rec- 
ognized. Contracted  visual  fields,  the  mental  state,  and  the 
ancesthesias,  if  associated  with  a  paralysis  not  characteristic 
of  organic  lesion,  are  sufficient  to  establish  the  diagnosis. 
But  occasionally  paralysis  occurs  as  the  only  symptom  of 
hysteria,  and  in  such  cases  the  elimination  of  shamming  is 
extremely  difficult.  Hysterical  paralysis  presents  the  one 
difference  that,  although  it  may  be  shown  by  hypnotism  to 
be  unreal,  it  does  not  fall  into  the  traps  which  so  frequently 
catch  the  simulator.  The  hysterical  patient  may  move  his 
leg  better  when  unobserved,  but  even  then  there  is  not  the 
complete  preservation  of  muscular  power  which  the  simula- 
tor may  be  shown  to  have. 

Tremor. — Tremor  is  a  symptom  of  nervous  disease 
which  is  very  difficult  of  simulation.  Attempts  to  imitate 
the  tremor  of  multiple  sclerosis  are  overdone.  It  is  doubtful 
if  the  tremor  of  paralysis  agitans  can  be  successfully  counter- 
feited for  any  length  of  time.  Even  if  it  were,  there  are 
so  many  other  symptoms  which  accompany  tremor  in  pa- 
ralysis agitans  that  it  may  be  regarded  as  practically  impos- 
sible to  feign  the  complete  clinical  picture  of  that  disease. 
The  gait,  the  facial  expression,  the  voice,  the  muscular  rigid- 


378 


MALINGERING. 


ity,  are  all  as  important  symptoms  of  paralysis  agitans  as 
tremor.  They  are  too  numerous  and  too  complex  to  permit 
of  consistent  and  simultaneous  mimicry.  The  other  pro- 
nounced tremors,  such  as  are  observed  in  paramyoclonus 
multiplex,  tic  convulsif,  etc.,  are  too  intricate  to  be  volun- 
tarily copied  with  any  degree  of  similarity.  Fine  tremor, 
either  in  the  face,  tongue,  or  hands,  is  a  common  symptom 
of  functional  nervous  disorders.  It  is  almost  identical  in 
character  with  the  trembling  observed  in  alcoholism  or  in 
excessive  tea  drinkers.  Although  it  can  not  be  voluntarily 
imitated  with  success,  it  is  well  to  bear  in  mind,  in  examin- 
ing any  case  which  presents  this  symptom,  that  it  may  de- 
pend on  conditions  which  antedated  the  accident. 

Anaesthesia. — In  organic  diseases  of  the  nervous  system 
anaesthesia  may  be  a  most  valuable  and  certain  symptom. 
In  diseases  of  the  peripheral  nerves,  in  spinal-cord  lesions, 
and,  to  a  less  extent,  in  cerebral  affections,  blunting  or  loss 
of  one  or  all  forms  of  sensory  function  is  of  the  highest 
value  for  purposes  of  diagnosis  and  localization.  It  may 
also  be  a  pathognomonic  evidence  of  hysteria.  The  signifi- 
cance of  this  symptom  can,  however,  be  easily  misinter- 
preted. Loss  of  cutaneous  sensibility  is  extremely  change- 
able in  functional  disorders,  and  even  in  organic  disease  it 
may  vary  considerably,  so  that  examinations  on  different 
days  or  at  different  times  of  the  same  day  do  not  yield  iden- 
tical results.  The  value  of  anaesthesia  as  an  objective  symp- 
tom is  further  impaired  by  the  fact  that  sensibility  varies  so 
extensively  in  degree  in  normal  individuals.  Women  are 
less  sensitive  to  pain  than  men.  Analgesia,  partial  or  com- 
plete, is  not  a  rare  occurrence  in  apparently  healthy  crimi- 
nals. Certain  races,  especially  the  Polish  Jews,  have  a 
variety  of  anomalies  in  pain  perception.  In  persons  who 
naturally  do  not  feel  pain  acutely  the  simulation  of  analgesia 
becomes  a  comparatively  easy  matter.  There  are  also  a 
good  many  individuals  who  can  suppress  any  evidence  of 


SIMULATION   OF   INDIVIDUAL   SYMPTOMS. 


379 


pain  as  long  as  their  attention  is  fixed  upon  this  object. 
Many  of  the  "  human  pincushions  "  in  museums  really  feel 
pain,  but,  in  consideration  of  the  salary  they  receive,  agree 
to  permit  an  inquisitive  public  to  stick  hat  pins  through  the 
calves  of  their  legs,  or  resort  to  similar  attempts  at  causing 
them  to  give  expressions  of  discomfort  or  suffering,  Knapp 
quotes  from  Pitres  a  case  of  this  kind  in  which  the  fraud 
was  exposed  :  "  A  man  had  for  several  years  taken  the  part 
of  the  anaesthetic  man  in  a  show,  enduring  pricks,  cuts, 
etc.,  without  the  slightest  manifestations  of  pain.  In  or- 
der to  obtain  the  shelter  of  hospital  life,  he  feigned  a 
disease,  one  symptom  of  which  was  anaesthesia ;  but  when 
he  was  subjected  to  the  unexpected  application  of  pain- 
ful stimuli,  Pitres  proved  at  once  that  the  anaesthesia  was 
feigned." 

Persons  whose  sensibility  to  pain  seems  normally  not 
highly  developed,  and  those  who  have  educated  themselves 
to  repress  any  of  the  ordinary  manifestations  of  pain,  have 
naturally  the  best  chance  of  escaping  detection  in  the  simu- 
lation of  ansesthesia,  and,  when  the  examination  is  not  thor- 
oughly and  thoughtfully  made,  may  lead  the  examiner  to 
believe  that  insensibility  really  is  present  ;  but  even  for 
these  cases  there  are  several  tests  which  will  generally 
prove  the  unreality  of  the  alleged  sensory  symptoms. 

In  all  sensory  examinations  the  eyes  should  be  blind- 
folded. Tests  for  analgesia  are  best  made  when  the  subject 
thinks  he  is  being  examined  for  something  else.  Thus,  if 
the  legs  are  alleged  to  be  anaesthetic,  a  sudden  thrust  of 
the  needle  into  one  leg,  while  the  operator  is  examining  the 
other,  may  cause  it  to  be  quickly  drawn  up.  Electrical  cur- 
rents are  usually  considered  of  value  for  the  detection  of 
feigned  analgesia.  They  may  be  applied  by  means  of  a 
strong  faradic  battery,  whose  current  strength  should  be 
suddenly  increased  without  the  knowledge  of  the  subject. 
Knapp  suggests  that  this  test  be  applied  during  the  course 


38o 


MALINGERING. 


of  the  ordinary  routine  of  electrical  examination  of  the  mus- 
cles. The  individual  muscles  may  be  examined  in  the  usual 
way,  and  then,  with  one  of  the  electrodes  over  the  alleged 
analgesic  area,  the  full  force  of  the  battery  is  suddenly 
turned  on.  Strong  faradic  currents  are  very  startling  and 
very  painful,  and  this  test  usually  results  in  some  sudden  ex-^ 
pression  of  surprise  and  suffering  if  the  insensibility  is  not 
genuine.  Detection  of  shamming  of  the  loss  of  sensibility 
to  touch  is  more  difficult.  The  person  whose  tactile  sensi- 
bility is  normal  will  know  if  there  has  been  no  contact  as  well 
as  recognize  light  touches  ;  but  he  can  deny  said  sensations, 
when  he  really  feels  them.  To  prove  his  statements  false  is 
not  always  possible.  The  test  usually  employed  is  to  mark 
out  the  areas  in  which  insensibility  to  touch  is  said  to  exist, 
and,  after  an  interval  of  a  few  minutes,  to  repeat  the  ex- 
amination and  note  if  the  results  of  both  examinations  agree. 
This  test  appears  to  me  to  be  of  very  slight  value  for  the  de- 
tection of  simulation.  If  the  angesthetic  areas  measured  at 
different  times  agree  perfectly,  it  is  certain  evidence  that 
there  is  some  serious  sensory  disturbance;  but  it  is  not  a. 
proof  of  feigning  if  the  limits  of  the  loss  of  sensibility  to 
touch  vary  somewhat  at  different  times.  Any  one  accus- 
tomed to  making  examinations  of  cutaneous  sensation  will 
remember  how  often  he  has  been  baffled  in  trying  to  make 
out  the  anassthetic  limits  in  cases  of  unquestionable  organic 
disease.  They  vary  so  widely  at  different  examinations  that 
variation  alone  is  not  sufficient  cause  for  the  assertion  that 
they  are  not  genuine.  Sensation  to  touch  is  essentially  a 
subjective  symptom  and  its  reality  is  very  difficult  to  prove. 
Since,  however,  in  simulation  its  loss  is  nearly  always  asso- 
ciated with  analgesia,  if  it  can  be  shown  that  the  patient  feels 
pain  when  he  says  he  does  not,  we  are  justified  in  assuming 
that  the  loss  of  touch  sense  is  also  false. 

Thermo-anassthesia   is   rarely   feigned.     To   test   for   its 
reality,  the  patient,  while  being  examined  with  the  test  tubes 


SIMULATION    OF   INDIVIDUAL   SYMPTOMS.  381 

filled  with  cold  water  and  warm  water,  may  suddenly  be 
touched  with  a  tube  of  boiling  water. 

None  of  these  tests  for  sensation  decide  positively  be- 
tween simulation  and  hysteria.  Through  the  suggestion 
imparted  by  manipulation  and  examination,  hysterical  anaes- 
thesia may  change  its  boundaries  or  change  its  situation^ 
or  entirely  disappear. 

It  can,  however,  usually  be  decided  in  accident  cases 
whether  the  anaesthesia  be  true  or  false  without  the  employ- 
ment of  these  tests,  which  are,  after  all,  suggestive  of  the 
methods  of  the  Inquisition. 

In  every  nervous  disorder  of  which  it  is  a  symptom,  an- 
aesthesia has  certain  peculiarities  of  character  and  distribu- 
tion as  well  as  of  the  way  in  which  it  is  associated  with 
other  symptoms.  These  are  individual  characteristics  fa- 
miliar only  to  those  who  have  devoted  considerable  study 
to  the  physiology  and  disease  of  the  nervous  system.  Were 
a  simulator  familiar  with  them — which  he  rarely  is — it  is 
extremely  improbable  that  he  could  put  his  theoretical 
knowledge  to  practical  use  during  a  thorough  medical  ex- 
amination. 

When  anaesthesia  follows  the  course  of  the  peripheral 
nerves,  or  the  sensory  distribution  of  the  spinal  segments,, 
or  occupies  areas  which  are  known  to  be  favorite  locations 
for  the  insensibility  of  hysteria,  it  furnishes  by  its  distribu- 
tion very  strong  presumptive  evidence  that  it  is  not  feigned  ;: 
but  when,  instead  of  being  characteristic,  it  assumes  a  form 
not  in  agreement  with  the  other  symptoms  present,  it  should 
at  once  arouse  suspicion  as  to  its  genuineness.  Such  a  sus- 
picion may  then  be  verified  by  the  tests  commonly  employed 
to  discover  if  the  anaesthesia  is  real  in  the  places  in  which  it 
is  alleged  to  exist. 

The  anaesthetic  areas  and  the  characteristics  of  anesthe- 
sia resulting  from  injuries  to  the  peripheral  nerves  or  to  the 
central  nervous  system  and  from  the  mental  state  of  hyste- 


382 


MALINGERING. 


ria  have  already  been  described  and  illustrated.  It  has  been 
emphasized  that  complete  loss  of  sensibility  rarely  follows 
peripheral-nerve  or  cerebral  injuries.  Since  the  sensory 
distribution  of  the  spinal  cord  has  become  almost  absolutely 
established,  it  is  just  as  possible  to  tell  from  the  anaesthesia 
what  segment  of  the  spinal  cord  is  injured  in  a  case  of  spi- 
nal compression  as  it  is  to  refer  the  numbness  and  tingling 
which  may  follow  a  peripheral  injury  to  the  nerve  upon 
whose  lesion  it  depends. 

If  in  any  case,  the  group  of  alleged  symptoms  point  to 
compression  or  injury  to  the  spinal  cord,  it  may  be  regarded 
■as  practically  impossible  for  the  simulator  to  have  sensory 
motor  and  reflex  symptoms  all  agree  so  that  they  could  be 
referred  to  injury  of  the  cord  at  or  below  any  one  segment. 
Thus,  to  again  quote  Case  III  of  Fannie  Freeman  the  fraud 
was  evident  from  the  anaesthesia  alone,  for  with  alleged 
total  paralysis  of  the  legs  the  anaesthesia  only  reached  the 
middle  of  the  thighs.  Such  a  localization  for  insensibility 
resulting  from  any  injury  to  the  spine  is  entirely  without 
precedent. 

The  irregular  areas  of  hysterical  anaesthesia  obey  certain 
general  laws.  In  traumatic  hysteria  the  loss  of  cutaneous 
sensibility  is  very  commonly  found  only  in  limbs  which  are 
paralyzed. 

To  distinguish  between  simulation  and  hysteria  by  the 
examination  of  sensation  alone  is  often  impossible.  As  in 
feigned  anaesthetic  areas,  so  in  parts  hysterically  anaesthetic, 
the  effects  of  accidental  injuries  to  the  skin,  so  common  in 
organic  anaesthesia,  are  rarely  observed.  In  feigned  anaes- 
thesia the  skin  bleeds  readily  ;  in  hysterical  anaesthesia  the 
skin  has  little  tendency  to  bleed  when  pricked.  But  usuall}^ 
by  reason  of  the  uncertainty  and  variability  of  the  sensory 
disturbances  of  hysteria,  it  is  necessary  to  look  for  associ- 
ated signs  before  one  can  be  certain  that  the  patient  really 
believes  he  does  not  feeL     In  traumatic  hysteria  such  addi- 


SIMULATION   OF    INDIVIDUAL   SYMPTOMS.  383 

tional  signs  are  usually  present,  and  it  is  by  appreciating 
the  character  of  hysterical  paralysis  or  contracture,  or  by 
demonstrating  a  functional  limitation  of  the  visual  fields,  that 
the  functional  character  of  the  anaesthesia  may  also  be  made 
plain. 

Pain  and  Hyperaesthesia. — It  is  very  difficult  to  deter- 
mine the  extent  and  true  character  of  alleged  pain.  In 
many  cases  disturbances  of  nutrition  and  the  general  bear- 
ing of  the  patient  permit  no  doubt  of  its  reality  ;  but  be- 
cause the  visible  evidences  of  suffering  are  absent  it  can 
not  always  with  certainty  be  inferred  that  the  patient  does 
not  suffer.  If  he  is  so  situated  that  he  can  be  constantly 
watched  in  order  that  it  may  be  determined  whether  the 
sleep  is  disturbed  or  the  expressions  of  pain  cease  when 
the  patient  thinks  himself  unobserved,  the  question  may  be 
decided  with  certainty.  In  negligence  cases  such  opportu- 
nities are  rarely  at  hand,  and  to  decide  how  much  the  pa- 
tient suffers  (or  if  he  suffers  at  all),  the  physician  must  usu- 
ally consider  each  of  the  many  factors  in  the  case,  of  which 
the  possible  motive  for  simulation,  the  general  bearing  of 
the  patient,  and  the  agreement  of  his  description  with  the 
ordinary  clinical  types  of  pain,  are  the  most  important. 
The  examination  should  be  as  long  as  is  feasible,  in  order 
to  find  out  if  the  pain  appear  to  be  continuous,  or  if  by  dis- 
traction of  the  attention  the  patient  can  be  made  to  betray 
himself. 

Hyperaesthesia  presents  many  of  the  same  difficulties  of 
diagnosis  as  pain.  Even  when  due  to  actual  nervous  dis- 
ease, it  is  more  intense  when  the  patient's  attention  is  fixed 
upon  it.  However,  when  any  one  who  makes  assertions  of 
extreme  sensitiveness  in  any  part  does  not  show  evidences 
of  pain  when  the  part  is  touched  without  his  being  fore- 
warned, it  is  very  probable  that  the  hyperaesthesia  is  exag- 
gerated or  feigned,  although  we  can  not  always  deny  posi- 
tively that   it   exists  because  the  patient  does  not  cry  out 


384  MALINGERING. 

when  the  sensitive  part  is  disturbed.  The  Mannkopff  symp- 
tom is  not  sufficiently  certain  in  its  action  to  permit  the  con- 
clusion that  pain  is  not  caused  by  pressure  on  alleged  sensi- 
tive parts  because  it  is  not  followed  by  an  increase  in  the 
heart's  action. 

Ocular  Symptoms. — Visual  disturbance  is  frequently  al- 
leged by  simulators,  but  they  usually  limit  themselves  to  the 
feigning  of  general  impairment  of  sight  or  of  blindness  in 
one  eye.  In  any  case  in  which  the  question  arises  as  to  the 
genuineness  of  blindness,  examination  by  an  ophthalmologist 
is  desirable.  Bilateral  blindness  imparts  such  characteristic 
features  of  attitude,  movement,  and  facial  appearance  that  a 
physician  who  is  at  all  familiar  with  morbid  ocular  conditions 
can  not  be  imposed  upon  for  any  length  of  time.  It  might 
be  possible  for  a  simulator  to  imitate  the  deportment  of  a 
blind  man  were  he  permitted  to  keep  his  eyes  closed,  but 
this  he  may  not  do.  Blind  men  keep  their  eyes  open  unless 
there  is  paralysis  of  the  ocular  muscles,  and  a  claimant  who 
kept  both  eyes  closed  would  immediately  arouse  suspicion. 
Furthermore,  in  true  blindness  there  are  important  altera- 
tions in  the  pupillary  reflex  and  in  the  fundus  of  the  eye. 
If  both  eyes  are  blind,  the  response  of  the  pupils  to  light  is 
impaired  or  lost.  If  one  eye  is  blind,  light  thrown  into  it 
does  not  cause  the  pupil  to  contract ;  but  if  light  is  thrown 
into  the  sound  eye,  the  pupil  of  the  blind  eye  contracts 
through  the  agency  of  the  consensual  reflex.  The  ophthal- 
moscope renders  valuable  information,  because  total  blind- 
ness rarely  occurs  in  one  or  both  eyes  without  there  being 
some  demonstrable  lesion  of  the  eye  itself.  If  such  a  condi- 
tion could  occur,  it  would  be  accompanied  by  other  evi- 
dences of  disease.  Although  in  locomotor  ataxia  there  may 
be  loss  of  perception  of  light  before  the  optic  atrophy  be- 
comes apparent,  examination  shows  a  loss  of  knee-jerk,  or 
ataxia,  or  other  signs  of  tabes. 

Atropine   or   allied    drugs   are  sometimes   used    by   im- 


SIMULATION   OF   INDIVIDUAL   SYMPTOMS. 


385 


posters  to  cause  a  dilatation  of  the  pupil  or  a  loss  of  the 
pupillary  reflexes.  Applied  either  locally  or  taken  inter- 
nally, atropine  may  cause  mydriasis,  with  immobility  of  the 
pupil  to  all  stimuli,  without  inducing  any  constitutional 
symptoms.  From  the  paralysis  of  accommodation,  vision 
for  near  objects  is  lost.  The  patient  can  not  read,  and  is 
uncertain  in  gait.  The  pupils  are  dilated,  and  do  not  change 
their  size  under  the  influence  of  light.  By  the  dilatation  of 
the  pupil,  however,  is  furnished  an  opportunity  for  the  more 
thorough  examination  of  the  fundus  of  the  eye.  Bilateral 
mydriasis  and  pupillary  immobility,  if  not  artificially  in- 
duced, are  almost  always  accompanied  with  significant 
changes  in  the  fundus,  discoverable  by  the  ophthalmoscope, 
or  by  paralysis  of  the  oculo-motorial  nerves,  or  by  evidences 
of  constitutional  conditions. 

The  feigning  of  monocular  blindness  may  be  discovered 
in  a  variety  of  ways.  If,  with  both  eyes  open,  a  prism  is 
placed  before  the  sound  eye  so  as  to  cause  diplopia,  and 
the  patient  admits  seeing  two  objects,  it  is  evident  that  he 
sees  one  of  them  with  the  eye  alleged  to  be  blind. 

This  test  may  be  rendered  more  delicate  by  bringing  the 
edge  of  the  prism  over  only  one  half  of  the  pupil  of  the  sound 
eye  while  the  other  eye  is  closed.  The  patient  at  once  ad- 
mits seeing  double.  Then  if,  after  uncovering  the  alleged 
blind  eye,  the  prism  is  held  directly  in  front  of  the  sound  eye, 
the  patient  admits  diplopia,  it  is  certain  proof  that  he  sees 
with  the  eye  alleged  to  be  blind.  Again  :  when  in  a  normal 
person,  one  eye  is  closed,  and  a  pencil  is  held  two  or  three 
inches  from  the  printed  page,  a  part  of  the  field  of  vision  is 
obscured  so  that  he  can  not  read  a  line  of  the  print  con- 
tinuously, although  with  both  eyes  open,  it  can  be  read  per- 
fectly well ;  consequently,  if  a  pencil  or  a  similar  object  be 
held  before  the  sound  eye,  and  the  patient  reads  the  lines 
continuously,  it  may  at  once  be  inferred  that  he  sees  with  the 
€ye  alleged  to  be  blind.     Or,  again,  if,  while  the  patient  is 


2  35  MALINGERING. 

reading  with  both  eyes  open,  a  strong  convex  lens  be  placed 
before  the  sound  eye  so  that  vision  with  it  becomes  im- 
possible, sight  may  be  proved  to  exist  in  the  alleged  blind 
eye  by  the  person  under  examination  continuing  his  reading. 
There  are  several  tests  with  colors.  Thus,  if  a  patient, 
with  both  eyes  open  and  with  a  red  glass  over  the  sound 
eye,  can  read  a  line  of  letters  made  with  a  red  pencil  on  a 
white  ground,  he  does  so  with  the  alleged  bhnd  eye,  since 
solid  red,  without  individualization  of  letters,  is  all  that  is 
seen  with  the  sound  eye.  Similarly,  with  both  eyes  open,  a 
spectacle  frame  containing  red  glass  on  one  side  and  green 
glass  on  the  other  is  placed  before  the  patient's  eyes.  He  is 
then  asked  to  read  the  test  cards  on  which  are  alternate  red 
and  green  letters,  large  at  one  end  and  growing  small  at  the 
other,  on  a  black  ground.  A  patient  who  has  binocular  vis. 
ion  can  read  these  letters  continuously,  but  a  patient  blind  in 
one  eye  would  miss  every  other  letter,  the  eye  which  is  cov- 
ered with  a  red  glass  seeing  only  the  red  letters,  the  green 
letters  being  neutralized  by  the  red  glass,  and  vice  versa. 

There  are  a  number  of  optical  arrangements  which  are 
resorted  to  for  the  detection  of  simulation.  The  stereoscope 
may  prove  of  service.  Also  the  boite  de  flees,  by  which  test 
the  subject  looks  with  both  eyes  into  a  box  containing  an 
optical  contrivance  by  means  of  which  the  object  that  is  ap- 
parently seen  by  the  right  eye  is  in  reality  seen  by  the  left 
one,  and  vice  versa  ;  so  that  a  simulator  may  admit  seeing  an 
object  which  appears  to  him  on  the  same  side  as  his  sound 
eye,  but  which  is  in  reality  seen  by  the  eye  said  to  be  blind. 
If  a  clever  simulator  makes  a  study  of  any  of  these  tests,  he 
may  become  sufficiently  expert  to  avoid  being  caught  by 
them. 

As  has  repeatedly  been  emphasized,  the  sight  is  in  reality 
not  lost  in  hysterical  blindness,  and  the  hysterical  patient 
may  be  regarded  as  a  simulator  because  he  does  not  conduct 
himself  during  the  above  tests  as  a  person  would  who  was 


SIMULATION   OF   INDIVIDUAL   SYMPTOMS.  387 

really  blind.  The  question  arises,  How  is  simulated  blind- 
ness to  be  distinguished  from  hysterical  blindness  ?  It  may 
often  happen  that  such  a  diagnosis  presents  many  difficulties, 
and  depends  for  its  solution  upon  associated  symptoms 
rather  than  upon  any  local  conditions.  Interferences  of 
vision,  of  which  the  patient  is  himself  conscious,  are  among 
the  more  serious  incidents  of  hysteria,  and  are  usually  ac- 
companied with  other  pronounced  hysterical  manifestations. 
If  in  any  case  of  blindness  which  is  not  organic  in  origin 
there  are  associated  and  well-marked  stigmata  of  hysteria, 
we  may  infer  that  the  blindness  also  depends  upon  actual  im- 
pairment of  vision  and  is  not  fraudulent ;  for  to  prove  fraud 
we  would  have  to  prove  that  the  general  symptoms  were 
also  feigned,  and  to  successfully  feign  the  complicated  clini- 
cal picture  of  hysteria  may  be  regarded  as  impossible. 

Limitation  of  the  visual  field  is  an  ocular  sign  of  great 
diagnostic  value  in  hysteria,  and  it  may  properly  be  regarded 
as  objective.  It  is  typical  of  hysteria,  and  probably,  in  this 
country  at  least,  is  never  feigned.  There  has  been  much 
discussion  among  European  neurologists  and  ophthalmolo- 
gists as  to  the  possibility  of  simulating  this  symptom.  It 
seems  possible  that  an  old  hospital  patient  who  had  assisted 
at  many  perimetric  examinations,  or  a  physician  who  had 
studied  visual  disturbances,  might  feign  limitation  of  the 
visual  fields.  But  the  perimeter  is  not  generally  popular  in 
this  country,  and  even  among  neurologists  is  infrequently 
used.  It  is  consequently  improbable  that  any  simulator  would 
take  the  trouble  to  learn  enough  about  this  symptom  to  coun- 
terfeit it  with  any  degree  of  success.  The  characteristics  of 
hysterical  contraction  of  the  visual  fields  have  already  been 
described,  and  need  not  be  repeated  here.  If  simulation  of 
it  were  attempted,  there  would  probably  result  irregularity 
and  inconsistencies  which  would  immediately  arouse  suspi- 
cion that  the  condition  was  not  genuine.  Knapp  suggests, 
if  the  case  is  in  any  way  doubtful,  the  use  of  perimeters  of 


^88  MALINGERING. 

different  diameters,  claiming  that  if  by  different  instruments 
the  fields  remain  the  same  the  contraction  is  not  feigned. 

If  the  patient  complains  that  his  eyesight  is  impaired 
but  not  lost,  it  is  more  difihcult  to  determine  how  much 
truth  there  is  in  these  statements.  If  examination  of  the 
■eye,  as  well  as  of  vision,  shows  no  abnormities,  the  decision 
as  to  whether  vision  really  is  impaired,  and  if  so  how  much, 
must  be  guided  by  the  other  aspects  of  the  individual  case. 

The  truth  can  usually  be  arrived  at  by  observing  the 
behavior  of  the  patient  during  protracted  examination,  in 
which  the  various  tests  for  acuity  and  extent  of  vision  are 
repeatedly  employed. 

Hearing. — Deafness  is  rarely  feigned  as  one  of  the  various 
nervous  symptoms  which  follow  accidents.  Hysterical  deaf- 
ness usually  occurs  in  the  form  of  impairment  of  hearing. 
If  the  patient  declares  he  is  absolutely  deaf  and  there  are 
no  evidences  of  any  structural  disturbance  in  the  auditory 
apparatus,  the  deafness  is  either  functional  or  feigned.  If 
feigned,  its  character  may  usually  be  disclosed  by  resorting 
to  the  various  tests  which  depend  upon  confusing  the  simu- 
lator or  taking  him  off  his  guard.  Knapp  proposes  the 
following  modification  of  Coggins's  stethoscope  test:  A  bin- 
aural stethoscope,  with  tubes  several  feet  long,  is  placed  in 
the  ears  of  the  person  to  be  examined.  The  tubes  should 
be  so  arranged  that  either  of  them  may  be  closed  at  the  will 
of  the  examiner  without  the  knowledge  of  the  subject.  Thus 
the  sound  may  be  conducted,  as  the  examiner  pleases,  to 
either  the  normal  or  the  alleged  deaf  ear,  which  may  lead 
the  simulator  to  make  contradictory  statements. 

Convulsive  Attacks. — The  convulsive  attacks  of  hysteria 
are  not  frequent  when  the  disorder  results  from  traumatic 
•causes,  and  when  they  occur  they  are  accompanied  with 
pronounced  permanent  stigmata,  and  can  easily  be  recog- 
nized at  their  true  value.  The  feigning  of  epilepsy  is  a  fre- 
quent device  among  criminals,  and  in  a  few  cases  epilepsy 


SIMULATION    OF    INDIVIDUAL   SYMPTOMS. 


389 


has  been  proved  to  be  simulated  in  actions  for  personal  in- 
juries. There  are  several  characteristics  about  epilepsy 
which  make  it  very  difficult  to  simulate  in  accident  cases. 
In  the  first  place,  epileptic  fits  only  occasionally  occur  in 
public.  Although  from  ten  to  fifteen  cases  of  epilepsy  are 
treated  daily  at  the  Vanderbilt  Clinic,  an  epileptic  fit  rarely 
takes  place  there,  and  we  are  obliged  to  treat  many  cases  of 
epilepsy  in  which  there  is  no  proof,  except  the  statement  of 
the  patient  or  his  friends,  that  epilepsy  exists.  The  epileptic 
paroxysm  follows  a  regular  cycle.  The  patient  falls,  irre- 
spective of  any  danger  of  hurting  himself ;  the  initial  mus- 
cular contractions  are  intense ;  the  face  is  blue ;  the  tongue 
is  bitten  ;  the  pupils  do  not  react  to  light ;  the  urine  is  passed 
involuntarily;  and  the  knee-jerks  are  lost  for  some  time  after 
the  convulsion  is  over. 

To  feign  epilepsy,  the  simulator  is  forced  to  have  his  at- 
tacks when  he  can  be  observed.  That  fits  can  be  shammed 
so  skillfully  that  they  might  pass  for  true  epilepsy  if  made 
before  a  witness  who  was  not  a  physician,  is  unquestionable. 
In  such  cases  it  is  impossible  to  tell  whether  the  person 
really  has  epilepsy  witliout  having  him  observed  by  some 
one  familiar  with  the  disease ;  then  the  fraud  can  usually  be 
discovered.  When  the  simulator  falls  he  usually  falls  in 
such  a  way  that  he  is  in  no  danger  of  being  hurt.  He  takes 
good  care  that  his  tongue  is  not  bitten  ;  there  are  no  changes 
in  the  reflexes  or  in  the  pupils ;  the  muscular  contractions 
are  exaggerated  and  theatrical ;  the  tonic  stage  is  usually 
very  short ;  and  in  the  clonic  stage  the  movements  have  a 
more  varied  and  unnatural  character  than  in  epilepsy. 

Vascular  Disturbances. — Voluntary  control  of  the  action 
of  the  heart  is  possessed  by  so  few  persons  and  always  in  so 
slight  a  degree,  that  the  simulation  of  tachycardia  merits  no 
particular  attention.  It  should  be  remembered,  however, 
that  rapid  and  tumultuous  heart  action  is  frequently  ob- 
served in  persons  who  have  no  serious  trouble  with  the 
26 


2go  MALINGERING. 

heart,  but  results  from  various  emotional  and  toxic  causes.. 
So  many  exciting  influences  attend  the  physical  examination 
of  the  chest,  especially  in  women,  that  considerable  care  and 
repeated  examinations  are  necessary  before  any  serious  sig- 
nificance can  be  attributed  to  tachycardia  when  it  is  unasso- 
ciated  with  other  symptoms  of  vascular  disturbance.  In 
simulation,  fear  of  detection  may  cause  the  heart  to  beat 
much  more  rapidly  ;  thus,  at  the  end  of  the  last  examination,. 
Fannie  Freeman's  pulse  rate  rose  to  132  to  the  minute,  al- 
though at  the  beginning  it  was  only  104. 

In  all  cases  in  which  there  is  any  tendency  to  rapid  or 
tumultuous  heart  action  the  examination  should  be  repeated 
after  the  patient's  first  excitement  has  passed  away,  or  after 
rest  in  the  recumbent  posture  has  permitted  a  re-establish- 
ment of  the  normal  cardiac  rhythm. 

The  other  vascular  symptoms,  such  as  flushings,  cold- 
ness, and  blueness  of  the  extremities,  can  not  be  counter- 
feited in  a  way  to  deceive  an  examiner  who  is  on  the  alert 
for  deception. 

Paralysis  of  the  Sphincters. — A  person  who  has  lost 
voluntary  control  of  the  bladder  or"  rectum  is  in  so  miser- 
able a  condition  that  a  superficial  examination  is  usually 
adequate  to  reveal  the  genuineness  of  the  symptoms.  Pa- 
ralysis of  the  bladder  results  in  retention  or  incontinence 
of  urine.  In  retention  the  urine  collects  until  it  is  drawn 
off  by  a  catheter,  or  until  the  filling  of  the  bladder  causes 
a  relaxation  of  the  vesical  sphincter,  so  that  the  urine  over- 
flows either  continuously  by  drops,  or  in  larger  quantities  at 
short  intervals  (overflow  incontinence).  In  incontinence 
the  lips  of  the  meatus  are  constantly  wet  from  the  continu- 
ous dribbling  of  the  urine.  Both  conditions  are  liable  to  be 
quickly  complicated  by  excoriations  on  the  scrotum  and 
sides  of  the  legs,  and  in  both  there  is  almost  unexceptionally 
a  strong  urinary  odor  about  the  bedding  and  about  the  pa- 
tient.    These  secondary  results  are  usually  absent  in  simu- 


SIMULATION   OF   INDIVIDUAL   SYMPTOMS.  391 

lation,  although  of  course  the  simulator  may  produce  them 
if  he  will. 

If  retention  is  alleged,  it  may  be  impossible  to  prove  it 
genuine,  unless  the  patient  can  be  watched  for  twenty-four 
hours,  in  order  that  it  may  be  observed  whether  or  not  he 
passes  water  involuntarily  and  exhibits  the  physical  signs  of 
a  distended  bladder.  Such  observation  is  often  impossible. 
Without  it  the  absence  of  the  ordinary  secondary  effects  of 
urinary  incontinence,  the  absence  of  distention  of  the  blad- 
der as  shown  by  percussion  above  the  pubes,  and  the  in- 
congruity of  the  associated  symptoms  with  the  alleged  vesi- 
cal condition,  are  usually  sufficient  for  diagnosis. 

False  incontinence  is  more  easily  detected  than  false  re- 
tention. In  the  absence  of  an  almost  constant  moistening  of 
the  meatus,  and  without  the  excoriations  and  urinary  smell, 
which  are  the  unavoidable  consequences  of  the  incontinence 
of  urine,  the  existence  of  that  condition  can  be  positively 
denied. 

Incontinence  of  faeces  is  easily  recognized.  In  addition 
to  the  faecal  odor  and  frequent  soiling  of  the  linen,  the  anal 
orifice  is  large  ;  and  when  the  examiner  inserts  the  finger  in 
the  rectum,  there  is  total  absence  of  the  normal  muscular 
contraction  of  the  sphincter. 

Reflexes. — The  reflexes  are  beyond  voluntary  control. 
The  skin  reflexes  can  not  even  be  modified.  In  cutaneous 
areas  which  are  insensitive  to  touch  or  pain  through  organic 
disease  or  through  hysterical  ideas  the  superficial  reflexes 
are  lost.  It  is  this  latter  fact  which  reacts  to  the  simulator's 
disadvantage,  for  if  they  are  not  lost  in  places  alleged  to 
be  anaesthetic,  it  should  excite  suspicion  of  shamming.  The 
cilio-spinal  reflex  and  the  tendon  reflexes,  on  the  contrary, 
continue  to  act,  unless  their  spinal  centers  or  their  con- 
ducting paths  have  been  destroyed.  The  tendon  reflexes 
often  appear  increased  in  suspicious  cases.  The  tap  on  the 
patellar  tendon  or  on  the  wrist  may  be  followed  by  a  con- 


OQ2  MALINGERING. 

traction  which  is  exaggerated  beyond  the  usual  limits.  If 
such  exaggeration  is  not  genuine,  it  usually  is  at  once  ap- 
parent by  the  momentary  pause  between  the  application  of 
the  stimulus  and  the  resulting  contraction.  A  person  who 
is  feigning  exaggeration  of  the  tendon  reflexes  may  be  at 
once  discovered  by  testing  them  when  his  eyes  are  covered. 
Deprived  of  vision,  he  can  no  longer  tell  when  to  expect  the 
tap,  and  the  pause  which  may  have  been  only  momentary 
when  his  eyes  were  open,  becomes  so  apparent,  and  the  con- 
traction is  so  evidently  unnatural,  that  there  is  no  difficulty 
in  saying  that  the  increase  is  feigned.  It  may  sometimes 
happen  that  the  tap  causes  the  natural  reflex  at  once,  and 
that  after  a  few  moments,  when  the  brain  has  had  time  to 
send  its  message,  a  second  contraction  occurs,  which  is 
manifestly  voluntary.  Foot  clonus  can  not  be  imitated  in  a 
way  to  deceive.  It  must  be  remembered  that  in  some  per- 
sons the  knee-jei-ks  are  naturally  very  active,  and  the  elbow- 
and  wrist-jerks  are  present ;  such  an  increase  is  always  bi- 
lateral and  is  of  little  significance. 

Like  the  superficial  reflexes,  the  tendon  reflexes  can  not 
be  decreased.  In  testing  for  the  knee-jerk,  if  it  fails  to  re- 
spond, it  will  be  found  that  the  knee  is  held  immobile  by  the 
muscles.  If  such  is  the  case,  the  flexor  tendons  of  the  leg 
will  be  felt  firm  and  hard,  preventing  any  extension  of  the 
leg.  The  Jendrassik  mode  of  re-enforcement  may  overcome 
this.  If  it  does  not,  it  must  be  said  that  the  patient  does  not 
permit  the  knee-jerks  to  be  tested,  but  not  that  they  are  lost. 

Bibliography. 

Bailey,  Simulation  of  Nervous  Disorders  following  Accidents. 
The  Railway  Surgeon,  February  8,  1896. 

Dana,  op.  cit. 

Godkin,  Accident  Cases.  Hamilton  s  System  of  Legal  Medicine, 
New  York,  1894. 

Heller,  Simulationen  und  ihre  Behandlung.     Leipzig,  1890. 

Hoffman,  Berl.  kl.  JVoch.,  June  21,  1891. 


SIMULATION    OF    INDIVIDUAL   SYMPTOMS. 


393 


Judd,  Legal  Aspects  of  Spinal  Concussion.  Boston  Med.  a7id 
Surg.  Joiir.,  1890,  vol.  cxxiii,  p.  219. 

Knapp,  Simulation  in  Traumatic  Nervous  Diseases.  Boston 
Med.  and  Surg.  Jour.,  September  28,  1893.  Ibid.,  Feigned  Diseases 
of  the  Mind  and  Nervous  System.  Hamilton's  System  of  Legal 
Medicine,  New  York,  1894. 

Page,  op.  cit. 

Prentice,  Speculation  in  Damage  Claims.  North  A?n.  Review, 
February,  1897. 

Prince,  Traumatism  as  a  Cause  of  Locomotor  Ataxia.  Jour. 
Nerv.  and  Me7ital  Dis.,  February,  1895. 

Schmidt-Rimpler,  Zur  Simulation  concentrischer  Gesichtfeld- 
einengung  mit  Berucksichtigung  der  traumatischen  Neurosen. 
Deut.  med.   Woch.,  1892,  p.  561. 

Schultze,  Dent.  med.  Zeit.,  October  16,  1891.  Ibid.,  Weiteres  iiber 
Nervenerkrankungen  nach  Trauma.  Dent.  Zeit.f.  Nervenh.,  1891, 
p.  444. 

Seeligmiiller,  Deutsch.  med.  Zeit.,  October  16,  1891. 


PART   IV. 

TREATMENT  OF  THE    TRAUMATIC  NEUROSES. 

It  has  been  frequently  asserted  in  preceding  pages 
that  the  prognosis  of  the  traumatic  neuroses  depends  in 
large  part  upon  the  ability  and  willingness  of  the  patient  to 
subject  himself  to  proper  treatment.  Although  the  present 
volume  concerns  itself  with  causes  rather  than  with  cures, 
it  seems  so  essential  that  there  should  be  a  greater  familiar- 
ity with  methods  which  can  often  prevent  a  reasonably 
healthy  man  or  woman  from  becoming  a  permanent  invalid, 
that  these  closing  pages  may  be  appropriately  devoted  to 
treatment.  As  we  have  seen,  these  disorders  comprise  trau- 
matic neurasthenia  and  traumatic  hysteria,  and  mixtures  of 
the  two.  The  treatment  for  all  is  essentially  the  same.  It 
consists  in  the  regulation  of  the  mode  of  life  in  such  a  way 
that  the  patient  is  shielded  from  those  influences  which  ex- 
perience has  shown  work  him  the  greatest  detriment,  and 
in  supplying,  as  far  as  possible,  the  essentials  of  normal 
healthy  living  which,  by  reason  of  fatigue  or  perverted 
ideas,  he  can  no  longer  gain  for  himself.  It  is  the  natural 
method,  rather  than  treatment  by  drugs,  and  it  is  based 
upon  principles  of  physiology  and  psychology,  rather  than 
upon  any  to  be  found  in  the  materia  medica.  Under  the  name 
of  the  Rest  Cure,  as  described  by  Weir  Mitchell,*  one  form 
of  treatment  for  neurasthenia  and  hysteria  is  generally 
familiar.  When  these  disorders  result  from  injury  or  shock 
it  undergoes  slight  modifications. 

*  Fat  and  Blood,  sixth  edition,  Philadelphia,  1891. 
394 


THE   REST   CURE. 


395 


The  Rest  Cure. — It  is  by  no  means  necessary  for  every 
case  of  traumatic  neurasthenia  or  hysteria  to  be  put  to  bed 
for  weeks  or  months.  It  is  advisable  for  any  one  who  has 
been  severely  frightened  or  shaken  up  to  rest  quietly  for  a 
few  days  or  a  week,  during  which  time  he  may  be  free  from 
effort  and  annoyance  and  have  his  thoughts  diverted  as 
much  as  possible  from  the  accident.  But  at  the  end  of  that 
time,  if  the  shock  and  bruising  were  not  excessive,  he  can 
usually  take  up  his  work  again.  When,  however,  neuras- 
thenia or  hysteria  is  pronounced,  and  especially  when  the 
patients  have  been  harassed  by  frequent  examinations  and 
have  found  no  benefit  from  various  therapeutic  methods, 
the  rest  cure,  in  its  most  comprehensive  extent,  remains  as 
the  best  means  of  speedy  if  not  of  ultimate  recovery. 

Before  proceeding  to  an  enumeration  of  the  various  pro- 
cedures incident  to  the  rest  treatment,  emphasis  must  be 
laid  upon  the  one  condition,  without  the  fulfillment  of  which 
success  is  imperilled  or  rendered  impossible.  This  condition 
is  the  complete  control  of  the  patient  by  the  physician.  The 
amount  of  rest,  both  physical  and  mental,  should  be  deter- 
mined by  him,  and  he  should  be  kept  constantly  informed 
of  the  most  trivial  happenings  which  go  on  in  the  sick-room. 
He  should  have  within  his  jurisdiction  the  regulation  of  the 
patient's  whole  mode  of  life  ;  he  should  have  the  right  to 
determine  whether  complete  isolation  be  necessary,  or  if  in- 
terviews with  friends  or  with  counsel  are  to  be  permitted, 
and  he  should  decide  as  to  their  frequency  and  their  length. 

While  litigation  is  pending  it  is  practically  useless  for 
the  patient  to  undertake  the  rest  cure.  Under  existing  con- 
ditions any  person  who  is  really  the  worse  for  an  accident 
can  usually  obtain,  by  settlement,  reasonable  compensation 
for  his  injuries  without  going  to  court.  If  the  claim  for 
damages  can  not  be  amicably  settled  without  suit,  the  patient 
may  as  well  decide  at  once  between  the  two  alternatives, 
viz. — whether  he  wishes  to  relinquish  the  chances  of  a  gen- 


39^ 


TREATMENT   OF    THE   TRAUMATIC   NEUROSES. 


erous  verdict,  or,  secondly,  to  indefinitely  postpone  his  re- 
covery. When  the  injuries  are  slight,  and  the  amount 
claimed  is  large,  this  decision  is  quickly  reached  ;  but  if  the 
functional  disorder  is  well  marked,  the  patient  is  often  un- 
able to  decide  for  himself.  Under  such  circumstances  the 
most  that  the  physician  can  do  is  to  explain  the  nature  of 
the  treatment,  and  to  show  how  impossible  it  is  to  fulfill  its 
requirements  and  at  the  same  time  to  grant  to  attorneys  the 
proper  facilities  for  preparing  their  case.  When  he  has  em- 
phasized the  unquestioned  truth  that  the  longer  a  traumatic 
functional  disease  exists  the  more  difficult  it  is  to  cure,  when 
he  has  explained  that  during  the  months  or  years  that  these 
suits  are  dragging  through  the  courts  before  a  final  verdict 
is  reached  the  disease  is  taking  on  a  phase  for  which  no 
money  can  be  considered  adequate  compensation — when  the 
physician  has  made  these  facts  plainly  evident  to  the  patient 
and  his  friends,  he  can  do  no  more. 

Althousfh  litio^ation  constitutes  the  most  serious  obstacle 
to  the  institution  and  carrying  out  of  the  rest  cure,  it  is  not 
always  easy  to  convince  the  patient  or  his  friends  of  the  rea- 
sonableness of  the  method,  even  when  the  powerful  factor 
of  litigation  is  absent.  The  friends  of  the  patient  often  re- 
gard him  as  more  frightened  than  hurt,  and  the  patient  him- 
self resents  being  deprived  of  his  liberty.  He  may  accede 
to  the  physician's  demand  for  a  time,  but  becoming  tired 
of  forced  seclusion,  eventually  insists  either  upon  returning 
home  or  of  undertaking  some  more  radical  form  of  treat- 
ment. Or  his  friends  may  be  unwilling  to  give  him  over  to 
the  entire  charge  of  strangers  and  to  place  him  where  he  is 
no  longer  amenable  to  their  wishes  or  the  recipient  of  their 
sympathy  ;  or,  having  consented  to  the  separation,  soon 
change  their  minds  and  insist  upon  some  less  exacting 
method.  Yet,  unless  the  patient's  surrender  is  uncondi- 
tional, and  unless  he  agrees  to  continue  the  treatment  for  a 
reasonable  length  of  time,  the  hopes  of  cure  of  confirmed 


THE   REST   CURE. 


397 


neurasthenia  or  hysteria  are  slight.  If  treatment  is  begun 
and  given  up  at  the  end  of  a  few  days  or  weeks,  the  patient 
goes  back  to  his  original  environment  or  falls  into  the  hands 
of  quacks,  and  loses  what  little  he  may  have  gained. 

The  fundamental  principles  of  the  rest  cure  depend  upon 
isolation  and  rest  in  bed.  By  means  of  the  first  it  is  intended 
to  permit  a  restoration  of  normal  vitality  to  brain  cells, 
whose  function  have  become  disordered,  and  by  the  second 
to  supply  to  the  whole  body  the  rest  it  needs,  but  which, 
without  artificial  means,  it  does  not  obtain.  These  two 
means  operate  conjointly,  the  action  of  one  enhancing  and 
supplementing  the  effect  of  the  other.  Isolation,  in  many 
cases,  should  be  so  absolute  that  the  nurse,  and  perhaps  the 
masseur,  are  the  only  persons,  except  the  physician,  whom 
the  patient  sees.  The  most  effective  method  (the  one  advo- 
cated by  Dr.  Mitchell)  is  obtained  away  from  the  patient's 
home.  For  this  purpose  quiet  hotels  or  boarding  houses,  or 
private  hospitals,  or  public  hospitals  in  which  a  quiet  room 
can  be  obtained,  are  frequently  utilized.  The  setting  aside 
of  a  room  in  the  patient's  own  house,  to  which  none  but  the 
physician  and  his  assistants  are  to  be  admitted,  is  sometimes 
feasible,  although  it  is  rarely  advisable  when  strict  seclusion 
is  to  be  enforced,  and  is  altogether  less  desirable  than  for  the 
patient  to  be  placed  away  from  familiar  sounds  and  scenes. 
If  complete  isolation  is  necessary,  it  should  be  so  effected 
that  there  is  no  communication  whatsoever  with  the  outside 
world.  Then  both  family  and  friends  are  excluded,  and 
there  is  naturally  total  banishment  of  all  questions  of  busi- 
ness;  the  patient  neither  writes  nor  receives  letters;  the 
meals  are  brought  to  the  door  of  the  room  by  an  attendant 
and  handed  in  to  the  nurse.  Such  absolute  imprisonment  is 
only  occasionally  desirable  and  is  rarely  necessar}'-  for  a  long 
time.  The  physician  must  decide  by  the  character  of  the 
patient  and  by  the  gravity  of  the  symptoms  when  to  insti- 
tute it  and  when  to  stop  it.     He  must  also  use  his  judgment 


398 


TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 


as  to  the  kind  of  persons  he  permits  the  patient  to  receive, 
taking  care  to  admit  last  such  relatives  or  friends  as  are  con- 
spicuous by  lack  of  tact  or  by  emotional  tendencies. 

The  one  constant  companion  of  the  patient  during  the 
weeks  when  the  isolation  is  more  or  less  complete  is  the 
nurse.  Male  nurses  are  not  fitted  for  this  kind  of  work,  and 
the  female  nurse  must  have  some  special  qualifications,  and 
if  possible  some  experience  in  the  management  of  such  cases. 
It  is  more  important,  however,  for  the  nurse  to  realize  that 
the  neurasthenic  patient  is  really  ill  than  it  is  for  her  to  be 
intimately  familiar  with  every  detail  of  the  treatment ;  for 
the  way  that  the  rest  cure  is  to  be  carried  out  in  an  indi- 
vidual case  will  be  indicated  to  her  by  the  physician  when 
the  treatment  begins,  but,  unless  she  realizes  that  the  un- 
reasonableness, impatience,  and  fretfulness  of  the  patient  are 
the  voicings  of  disease,  she  will  be  unable  to  maintain  the 
gentleness,  firmness,  and  patience  upon  which  qualities  of 
the  nurse  the  success  of  the  rest  cure  depends.  No  task  is 
more  trying  than  the  care  of  such  patients  ;  it  requires  good 
health  and  an  even  temper;  it  is  easiest  for  those  nurses 
who  are  enduring  and  unemotional,  and  who  by  their  cheer- 
ful manners  and  ability  to  talk  or  read  well,  or  by  similar 
accomplishments,  can  make  the  time  pass  most  pleasantly 
and  quickly  for  their  bedridden  companions. 

Next  to  isolation,  and  together  with  isolation,  the  most 
important  feature  of  the  rest  cure  is  rest  in  bed,  the  com- 
pleteness of  which  varies  with  the  severity  of  the  case.  In 
grave  cases  of  neurasthenia  the  patient  is  kept  as  nearly  mo- 
tionless as  possible.  He  is  not  permitted  to  feed  himself, 
and  should  not  even  turn  over  in  bed  without  the  assistance 
of  the  nurse.  The  use  of  the  bedpan  and  of  the  portable  uri- 
nal renders  it  unnecessary  for  him  to  get  up  to  empty  the 
bowels  or  bladder.  Like  isolation,  this  enforced  rest  gener- 
ally proves  disagreeable  to  the  patient  for  the  first  few  days. 
However,  he  ordinarily  becomes  soon  accustomed  to  it,  and 


THE   REST   CURE. 


399 


ceases  to  complain.  When  the  time  arrives  for  complete 
inactivity  to  be  abandoned,  the  change  is  to  be  effected 
gradually.  At  first  the  patient  may  sit  up  in  bed  for  a  few 
minutes  at  a  time;  then  sit  with  the  feet  out  of  the  bed  rest- 
ing on  a  pillow  ;  then  sit  in  a  chair,  and  gradually  begin  to 
walk,  doing  a  little  more  each  day  than  he  did  the  day  pre- 
ceding. 

Although  the  re-establishment  of  the  exhausted  nervous 
system  is  best  secured  by  means  of  isolation  and  prolonged 
rest  from  voluntary  effort,  the  fact  remains  that  the  circula- 
tion is  more  active  and  nutrition  consequently  better  when 
the  muscles  do  some  work.  To  secure  muscular  activity 
without  making  serious  demands  upon  the  nervous  system, 
the  methods  at  our  disposal  are  massage  and  electricity. 
Massage  may  be  given  by  the  nurse  if  she  is  a  skillful  mas- 
seuse, and  then  no  outsider  need  be  introduced,  and  the  iso- 
lation of  the  patient  remains  undisturbed.  To  be  able  to 
give  massage  well,  however,  is  an  art  in  itself,  of  which  only 
a  few  of  the  graduates  of  our  training  schools  are  mistresses. 
The  most  skillful  masseurs  and  masseuses  that  we  have  in 
this  country  have  been  educated  in  this  special  branch  in 
Sweden,  and,  in  New  York  at  least,  confine  themselves  solely 
to  giving  massage.  If  the  passive  movement  is  to  be  given 
by  some  one  other  than  the  nurse,  it  adds,  of  course,  addi- 
tional expense  to  the  treatment,  and  diminishes  the  seclusion 
of  the  patient ;  but  the  value  of  systematic  and  skillfully  ap- 
plied massage  is  so  great  that  its  proper  administration  more 
than  counterbalances  these  drawbacks.  Systematic  rubbing 
of  the  whole  body,  for  purposes  of  general  nutrition,  must  be 
instituted  gradually,  as  the  idea  of  having  the  body  touched 
by  others  is  repulsive  to  many  persons,  and  most  patients 
only  become  accustomed  to  it  after  several  stances.  It  is 
best  to  delay  it  until  the  treatment  has  lasted  several  days, 
and  to  begin  it  by  merely  rubbing  an  arm  for  a  few  minutes. 
It  may  then  be  gradually  extended,  so  that  at  the  end  of  a 


400 


TREATMENT    OF   THE    TRAUMATIC   NEUROSES. 


week  or  ten  days  the  seances  last  an  hour,  and  the  arms^ 
legs,  abdomen,  and  back  are  being  systematically  exercised 
every  day. 

Electricity  is  the  other  means  by  which  the  patient  may 
obtain  exercise.  Its  effects,  although  less  pronounced,  are 
similar  to  those  of  massage.  If  a  good  masseur  or  mas- 
seuse can  be  obtained,  there  is  rarely  any  necessity  for  using 
electricity.  When  for  any  reason,  however,  it  is  impossible 
to  secure  the  services  of  a  skilled  massage  operator,  the  fara- 
dic  battery  can  be  successfully  substituted.  It  has  the  ad- 
vantage that  an  intelligent  nurse  can  be  easily  taught  to  use 
it  gently  and  effectively,  and  that  "  electrical  treatment " 
often  has  a  beneficial  mental  effect  on  the  patient.  The 
electrodes  should  be  wet  with  warm  salt  water,  and  as  the 
sponges  get  very  dirty,  it  adds  a  touch  of  neatness  to  the 
procedure  if  they  are  either  frequently  changed,  or  else  cov- 
ered by  pieces  of  white  gauze  at  the  time  of  each  application. 
At  first  the  current  is  applied  in  very  weak  strengths,  and 
to  small  areas  of  the  body  ;  as  the  patient  becomes  used  to 
its  action  the  current  strength  may  be  increased  until  the 
muscles  react  promptly  and  all  of  them  are  in  turn  stimu- 
lated.    The  stance  should  last  about  half  an  hour. 

The  regulation  of  the  diet  during  the  rest  cure  is  con- 
trolled by  two  considerations — viz.,  that  it  should  be  so  ar- 
ranged that  the  patient  may  receive  plenty  of  nourishment 
in  spite  of  any  gastric  irritability  that  he  may  have  ;  and,  sec- 
ondly, that  the  amount  of  food  taken  should  be  excessive 
and  out  of  proportion  to  the  work  which  is  done  (forced 
feeding).  If  at  the  beginning  of  the  treatment  dyspeptic 
symptoms — such  as  anorexia,  nausea,  vomiting,  and  eructa- 
tions— are  present,  the  alimentation  must  consist  exclusively 
of  milk,  in  order  that  the  stomach  may  be  brought  as  soon 
as  possible  to  a  condition  in  which  it  can  retain  large  quan- 
tities of  more  substantial  food.  Under  these  circumstances 
the  milk  is  given  in  very  small  quantities  which  are  repeated 


THE   REST   CURE. 


401 


at  short  intervals  during  waking  hours.  Thus,  one  or  two 
ounces  of  milk  given  every  hour,  or  slightly  larger  amounts 
given  every  two  hours,  are  sufficient  for  the  first  few  days. 
Administered  in  this  way,  milk  can  be  borne  by  almost  any 
one,  although  he  may  think  that  it  does  not  agree  with  him, 
and  although,  if  given  in  larger  quantities,  it  might  immedi- 
ately induce  an  attack  of  vomiting.  In  rare  instances  it 
may  seem  necessary  to  have  the  milk  peptonized.  Koumyss, 
on  account  of  the  alcohol  it  contains,  is  not  to  be  recom- 
mended as  an  exclusive  diet.  This  method  of  feeding,  com- 
bined with  the  rest  in  bed,  is  usually  sufficient  to  quiet  the 
more  prominent  of  the  gastric  symptoms  so  that  in  a  very 
short  time  the  quantities  of  milk  may  be  increased,  or  it 
may  be  alternated  with  more  palatable  articles  of  food.  At 
the  end  of  a  week  it  is  usually  possible  for  the  dietary  to  be 
amplified,  so  that  while  the  patient  continues  to  be  fed  every 
two  hours,  he  receives  substitutes  for  the  milk  two  or  three 
times  a  day.  These  substitutes  should  at  first  be  limited  to 
fluids,  such  as  soups  or  broths,  or  some  of  the  prepared 
foods ;  but  they  may  very  soon  be  made  to  include  soft- 
boiled  eggs,  custards,  and  jellies,  until  finally,  by  the  ad- 
dition of  chops,  steaks,  chicken,  etc.,  the  patient  is  receiving 
a  regular  diet.  As  long  as  he  remains  in  bed  the  plan  of 
some  nourishment  every  two  hours  should  be  adhered  to, 
although  no  large  quantity  may  be  taken  at  any  one  time. 
Even  after  he  gets  up  and  begins  to  walk  around,  and  is 
taking  three  fairly  full  meals  a  day,  he  should  have  some 
nourishment  between  meals,  in  order  that  the  amount  of 
food  taken  remain  excessive. 

Stimulants  should  be  as  far  as  possible  avoided.  Tea 
and  coffee  can  generally  be  excluded  without  difficulty.  To 
relieve  the  tedium  of  the  dietary  a  cup  of  cocoa  or  chocolate 
may  be  occasionally  permitted.  If  the  patient  is  markedly 
alcoholic,  with  symptoms  of  cardiac  weakness,  it  may  be 
necessary  to  provide  some   means  for  the  improvement  of 


402  TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 

the  heart's  action.  This  may  be  done  by  prescribing  small 
quantities  of  alcohol,  or,  better,  some  of  the  heart  tonics,, 
such  as  strychnine,  strophanthus,  or  digitalis.  Tobacco, 
while  the  patient  remains  in  bed,  is  to  be  avoided.  Later 
the  advisability  of  its  use  must  be  determined  by  the  effect 
it  has  on  the  individual.  If  it  renders  him  more  nervous, 
and  if  it  is  desired  to  use  it  in  excess,  it  should  be  cut  off 
altogether.  When,  however,  its  efiect  is  to  calm  rather 
than  to  excite,  one  or  two  cigars  a  day  can  with  safety  be 
allowed. 

The  general  management  of  a  neurasthenic  man  or 
woman  during  the  one  or  two  months  that  the  only  persons 
he  or  she  sees  are  comparative  strangers,  is  a  matter  of  con- 
siderable delicacy.  Although  the  patient  is  in  a  certain 
sense  a  prisoner,  he  has  undertaken  the  treatment  of  his  own 
accord,  and  he  can  terminate  it  when  he  wishes.  It  must 
accordingly  be  the  physician's  care  to  make  the  period  of 
confinement  as  little  irksome  as  is  consistent  with  the  ulti- 
mate object  in  view.  Every  possible  latitude  and  privilege 
consistent  with  the  sick  man's  welfare  he  should  endeavor 
to  provide.  When,  however,  it  has  once  been  decided  what 
the  patient  may  and  may  not  do,  the  plan  of  treatment 
should  remain  unaffected  by  unreasonable  protestations  and 
complaints.  By  acceding  to  demands  which  are  the  results 
of  fretfulness  and  impatience  the  physician  or  nurse  will 
seriously  lose  in  personal  influence,  and  will  postpone  the 
time  when  such  nervous  manifestations  are  to  permanently 
disappear.  Gentle  firmness  on  the  part  of  both  physician, 
and  nurse  is  essential  to  the  success  of  this  kind  of  treat- 
ment. Objections  and  complaints  are  best  forestalled  and 
obviated  by  instituting  at  once  a  daily  riginie  to  which  the 
patient  is  to  conform  as  regularly  as  though  he  were  keep- 
ing business  appointments.  By  this  means  he  comes  to  look 
forward  to  the  hours  given  up  to  special  things  with  ex- 
pectancy if  not  with  pleasure,  and  the  time  passes  with  rea- 


THE    REST   CURE. 


405 


sonable  rapidity.  When  the  daily,  or  rather  hourly,  sched- 
ule is  once  determined  upon,  it  should  only  be  changed  for 
purposes  of  enlargement.  Its  special  character  varies  with 
individual  cases,  but  its  principle  remains  essentially  the 
same.  Thus,  if  the  patient  does  not  leave  the  bed  at  all^ 
he  has  milk  at  seven ;  at  eight  he  is  assisted  at  his  toilet  by 
the  nurse  and  receives  a  sponge  bath  ;  at  nine  more  milk, 
and  is  read  to  for  a  short  time ;  at  ten  the  physician  calls ; 
at  eleven  more  nourishment,  followed  by  rest  and  quiet, 
and  so  on  throughout  the  day,  there  being  definitely  deter- 
mined hours  for  the  physician's  visit  and  that  of  the  mas- 
seur, for  reading,  talking,  resting,  eating,  etc.  As  the  pa- 
tient begins  to  improve,  these  hours  are  changed  to  fit  differ- 
ent requirements,  but  the  rule  of  regularity  remains  un- 
disturbed. 

The  length  of  time  necessary  for  the  observance  of  the 
more  stringent  requirements  of  the  rest  cure  is  in  large  part 
determined  by  the  rapidity  with  which  improvement  results 
from  the  treatment.  As  a  general  rule,  the  more  prominent 
symptoms  begin  to  yield  in  a  few  days  or  weeks.  As  a  re- 
sult of  the  milk  diet  the  dyspeptic  symptoms  disappear  and 
the  patient  begins  to  realize  that  he  has  an  appetite  ;  the 
sleep  becomes  improved  in  quality  and  in  duration ;  the 
pains  are  less  frequently  complained  of;  the  tremor  and  ex- 
citability are  less  evident;  the  nutrition  is  raised, as  is  shown 
by  an  increase  in  the  color  and  the  firmness  of  the  skin,  and 
by  a  gain  in  weight.  There  is  no  absolute  rule  by  which  it 
may  be  determined  just  when  the  patient  may  get  up  or  be- 
gin to  see  his  friends  again.  As  in  convalescence  from 
general  diseases,  this  question  must  be  decided  by  the  phy- 
sician who  has  learned  the  capabilities  of  the  person  under 
his  care,  and  who,  by  gradually  permitting  him  to  do  more 
and  more,  can  readily  ascertain  how  rapidly  the  return  to 
normal  living  should  be. 

Valuable  as  is  the  rest  cure,  it  is  not  infallible  ;  and  the 


404 


TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 


question  arises,  If  the  patient  improves  but  little  or  not  at 
all,  how  long  should  the  treatment  continue  ?  To  this  differ- 
ent answers  are  given  by  various  authors.  In  general  it 
may  be  said  that  if  at  the  end  of  two  months  the  benefit  is 
not  plainly  perceptible,  the  method  of  treatment  should  be 
very  much  modified  or  changed  altogether.  The  prognosis 
for  recovery  in  such  cases  is  far  from  bright. 

When  the  rest  cure  is  reasonably  successful,  at  the  end 
of  from  one  to  three  months  the  patient  is  comparatively 
free  from  the  distressing  symptoms  from  which  he  suffered 
at  its  beginning,  and  can  endure  a  moderate  amount  of  exer- 
tion fairly  well.  He  is  still  somewhat  nervous  and  excitable, 
however,  and  in  very  much  the  same  condition  as  many 
neurasthenics  who  are  hardly  ill  enough  to  need  the  rest 
cure,  but  who  require  some  special  form  of  treatment  for 
the  re-establishment  of  health. 

Carried  out  in  its  most  perfected  form,  the  rest  cure 
is  expensive,  as  it  implies  that  the  patient  be  away  from 
his  work  for  several  weeks  or  months,  that  he  be  con- 
stantly under  the  supervision  of  a  nurse,  and  frequently 
visited  by  a  physician.  An  effort  is  being  made,  how- 
ever, to  make  it  more  accessible  to  persons  who  are  in 
moderate  circumstances.  In  the  Philadelphia  Hospital  beds 
are  set  aside  for  this  treatment,  and  some  few  of  the  hos- 
pitals connected  with  the  railways  have  recognized  its  value, 
and  undertake  to  treat  patients  in  accordance  with  its  prin- 
ciples. 

In  persons  who  no  longer  require  the  complete  rest  cure, 
and  in  those  who  were  never  ill  enough  make  such  a  pro- 
cedure necessary,  rest,  more  than  is  necessary  for  healthy  in- 
dividuals, is  still  a  primary  requisite.  This  may  be  secured, 
if  the  patients  have  no  employment,  bv  not  rising  until  after 
breakfast,  and  by  lying  down  for  thirty  minutes  or  an  hour 
two  or  three  times  during  the  course  of  the  day.  If  it  is 
necessary  that  the  patient  return  to  his  employment — and 


HYDRIATRICS. 


405 


in  many  cases  such  a  course  is  extremely  desirable — rest 
ma)'-  sometimes  be  obtained  during-  working  hours  ;  or,  if 
not,  the  patient  should  go  to  bed  earlier  than  usual,  so  that 
he  passes  at  least  ten  hours  in  bed.  The  whole  mode  of  life 
of  a  neurasthenic  should  be  moderate  and  equable.  He 
should  shun  as  far  as  possible  all  that  may  fatigue  or  excite. 
What  has  been  said  in  regard  to  litigation  in  its  relations  to 
the  rest  cure  may  be  repeated  with  almost  equal  force  for 
the  patient  who  does  not  need  to  be  isolated  or  put  to  bed. 
In  the  first  case  it  is  a  bar  to  recovery  from  a  serious  condi- 
tion ;  in  the  second  it  exposes  the  patient,  who  under  proper 
conditions  might  soon  be  well,  to  the  danger  of  becoming- 
an  irritable  and  hopeless  invalid. 

There  are  a  variety  of  procedures  ^besides  the  rest  cure 
which  are  efficacious  in  the  amelioration  and  cure  of  neuras- 
thenic and  hysterical  conditions.  Some  of  them  are  ap- 
plicable during  the  rest  cure  itself,  and  some  are  only  re- 
sorted to  as  a  termination  of  that  form  of  treatment  or  in 
cases  which  are  not  sufficiently  severe  to  demand  seclusion 
and  forced  rest.  For  purposes  of  convenience  they  will  all 
be  considered  together. 

Hydriatrics. — Second  only  in  value  to  the  rest  cure  in 
the  treatment  of  neurasthenia  and  hysteria  is  the  scientific 
application  of  water.  Taken  internally,  by  causing  an  in- 
creased activity  in  the  kidneys  and  skin,  and  by  diluting  the 
toxic  metabolic  products  which  are  circulating  in  the  blood, 
it  exerts  a  most  beneficent  influence  upon  nutrition.  It  may 
be  administered  with  advantage  in  large  quantities  during 
the  whole  course  of  neurasthenia  or  hysteria,  with  the  ex- 
ception of  that  period  of  the  rest  cure  during  which  the 
patient  is  on  a  fluid  diet.  A  not  unpleasant  method  is  a 
glass  of  very  hot  water,  taken  one  hour  before  each  meal. 
It  is  the  external  application  of  water,  however,  which  is  at- 
tended with  the  most  brilliant  therapeutic  results  in  func- 
tional nervous  diseases. 
27 


4o6  TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 

Thirty  years  ago  the  water  treatment,  whose  ignorant 
exponents  were  called  ''  hydropaths,"  had  won  a  well-de- 
served reputation  for  quackery.  To-day,  largely  through, 
the  researches  of  Winternitz,  of  Vienna,  and  of  his  pupil,, 
Simon  Baruch,  of  New  York,  it  has  taken  its  place  among 
the  most  efficient  of  therapeutic  agents.  Its  importance  is. 
universally  admitted  in  Europe,  where  hydrotherapeutic 
establishments  are  numerous.  Among  the  most  prominent 
of  these  may  be  mentioned :  In  Austria,  Dr.  Winternitz's,  at 
Kaltenleutgeben,  near  Vienna ;  the  Centralbad,  in  Vienna  ; 
Dr.  Koehler's,  in  Eisenbach ;  Dr.  Pospischl's,  in  Krems  ;  in 
Germany,  at  Elgersberg  and  Konigstein  ;  in  France,  at  Di- 
vonne  and  Lamalou  ;  in  England,  at  Malvern. 

In  America,  although  the  recognition  of  the  usefulness 
of  hydriatrics  was  less  prompt  than  on  the  other  side  of 
the  ocean,  its  value  is  now  becoming  rapidly  appreciated. 
Some  of  the  sanitaria  in  this  country  are  prepared  to  ad- 
minister many  of  the  procedures  of  the  water  treatment. 
Prominent  among  these  institutions  are  the  ones  at  Dans- 
ville,  Clifton  Springs,  and  Watkins,  in  the  State  of  New 
York,  and  at  Battle  Creek,  Mich.  The  Hydriatric  Insti- 
tute in  New  York  city,  and  two  institutions  at  Louisville, 
Ky.,  are  fitted  out  with  complete  apparatus  for  all  hydriatric 
procedures,  the  various  douches  being  the  chief  applications 
made  in  them. 

The  institutions  at  Louisville,  the  Hydriatric  Institute 
and  the  Riverside  Public  Baths  in  New  York,  give  treat- 
ment to  ambulant  patients  who  may  return  to  their  homes 
after  each  treatment. 

The  beneficial  effects  of  wisely  chosen  hydrotherapeutic 
measures  are  especially  evident  in  the  functional  nervous 
diseases.  Since  the  opening  of  the  hydriatric  department 
of  the  Riverside  Public  Baths  in  New  York  city,  most  of 
the  Vanderbilt  Clinic  cases  of  neurasthenia  and  hj^steria  are 
referred  to  that  institution  for  cold  douches.     It  is  only  jus- 


HYDRIATRICS.  407 

tice  to  state  that  our  success  in  the  treatment  of  these  con- 
ditions is  now  much  more  satisfactory  than  it  previously  had 
been.  The  improvement  in  nervous  symptoms  which  often 
follows  a  sojourn  in  a  sanitarium  is  largely  due  to  the  water 
treatment  received  there.  Some  patients  with  neurasthenia 
and  hysteria,  in  whom  but  little  benefit  was  derived  from 
the  rest  cure,  have  returned,  apparently  well  in  every  way, 
after  a  few  months'  stay  at  a  sanitarium. 

The  success  of  hydrotherapy  in  any  case  depends  in 
large  part  upon  whether  the  proper  procedure  is  chosen  for 
the  individual  condition  it  is  meant  to  benefit,  and  upon 
whether  it  is  properly  carried  out.  The  methods  which 
have  proved  most  successful  in  the  treatment  of  the  func- 
tional nervous  diseases  may  be  briefly  outlined  here,  al- 
though for  a  thorough  comprehension  of  this  important 
subject  the  reader  must  be  referred  to  special  treatises.* 

The  sponge  bath,  which  is  given  daily  during  the  period 
of  the  rest  cure  when  the  patient  is  in  bed,  is  chiefly  for  pur- 
poses of  cleanliness.  Different  segments  of  the  body  are 
sponged  off  with  water  at  70°  F.  and  then  dried.  Each  seg- 
ment is  dried  and  wrapped  up  before  another  segment  is 
bathed. 

The  drip  sheet  is  to  be  used  when  the  patient,  after  the 
rest  cure,  is  beginning  to  walk  around  the  room.  The  best 
time  for  its  application  is  upon  rising  in  the  morning.  It 
has  the  advantage  that,  as  it  requires  no  special  apparatus,  it 
may  be  given  perfectly  well  at  home,  and  is  less  alarming 
to  the  patient  than  some  of  the  more  elaborate  hydriatric 
measures.  The  sheet,  after  having  been  partially  wrung 
out  in  water  at  seventy  degrees,  is  applied  as  follows  :  The 
nurse,  standing  behind  the  patient,  whose  head  has  been  wet 
with  cold  water,  puts  one  corner  of  the  sheet  under  the  pa- 
tient's right  arm  and  carries  it  across  the  chest ;  the  rest  of 

*  See  Baruch  on  Hydrotherapy,  in  Hare's  System  of  Therapeutics,  Philadel- 
phia, 1 891. 


4o8  TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 

the  sheet  is  then  carried  across  the  back,  over  the  left  shouL 
der,  and  continued  over  the  front  of  the  right  shoulder  until 
the  end  can  be  tucked  in  at  the  back,  so  that  the  body  is  en- 
tirely covered.  By  slapping  and  by  light  and  rapid  rubbing 
over  the  sheet,  from  periphery  toward  the  center,  the  pa- 
tient soon  becomes  warm.  When  the  reaction  is  fully  estab- 
lished, which  occurs  in  one  or  two  minutes,  he  is  dried 
off  quickly  with  a  towel  and  returned  to  bed.  In  succeed- 
ing applications  the  temperature  of  the  water  may  be  re- 
duced a  few  degrees  at  a  time  until  it  finally  reaches  fifty 
degrees. 

The  Wet  Pack. — The  full  wet  pack  is  only  occasionally 
necessary  in  the  functional  nervous  disorders.  When  neces- 
sary, the  patient  is  wrapped  in  a  sheet  wrung  out  in  water 
at  seventy  degrees — which  may  be  daily  reduced  one  degree 
in  temperature  until  sixty  degrees  is  reached — and  then 
rolled  in  a  blanket,  in  which  he  is  left  for  an  hour  or  longer. 
This  procedure  is  of  especial  service  when  insomnia  is  pro- 
nounced or  when  the  nervous  symptoms  are  in  large  part 
dependent  upon  alcoholism  or  upon  inadequate  elimination 
by  the  kidneys,  and  in  erethetic  conditions.  More  frequent- 
ly the  desired  results  may  be  obtained  by  the  local  wet  pack, 
which  is  one  of  the  most  efficient  agents  for  allaying  mental 
excitement  and  inducing  sleep.  It  is  also  often  useful  in  the 
treatment  of  chronic  constipation.  It  is  applied  by  placing 
a  piece  of  sheet  folded  two  or  three  times,  which  has  been 
thoroughly  wrung  out  in  water  at  sixty  to  seventy  degrees, 
and  then  folded  in  the  form  of  a  compress  across  the  pa- 
tient's abdomen.  A  piece  of  flannel  bandage  of  the  same 
length  as  the  compress,  but  two  inches  wider,  is  then  put 
around  the  body,  so  that  it  holds  the  compress  in  position. 
The  abdominal  compress  is  usually  applied  just  before  going 
to  bed,  and  should  be  left  for  half  an  hour.  If  at  th€  expira- 
tion of  this  time  no  effects  from  its  use  are  apparent,  the 
sheet  may  be  wrung  out  in  cold  water  and  again  applied. 


HYDRIATRICS. 


409 


The  Foot  Bath. — In  hydriatric  institutions  the  water  for 
the  foot  tub  enters  and  leaves  in  a  constant  and  rapid  stream, 
so  that  there  is  the  stimulus  of  mechanical  irritation  as  well 
as  that  of  heat  or  cold.  In  private  houses  it  is  usually  neces- 
sary to  be  content  with  an  ordinary  foot  tub  filled  with 
water  at  the  desired  temperature.  The  patient  sits  with  the 
feet  in  the  water,  which  comes  above  the  ankles.  Either  hot 
or  cold  water  may  be  used,  the  effects  of  each  being  similar. 
In  the  cold  foot  bath  the  water  is  at  a  temperature  of  forty 
degrees,  and  the  patient  rubs  the  feet  energetically  one 
against  the  other  for  about  five  minutes.  By  the  friction 
the  feet  are  kept  comfortably  warm.  While  in  the  water, 
and  when  they  are  taken  out,  their  capillaries  undergo 
marked  dilatation,  as  is  shown  by  the  rosy  color  of  the  skin 
and  the  sensations  of  warmth  in  the  lower  extremities.  The 
hot  foot  bath  is  on  the  whole  less  efficacious,  although  often 
very  useful.  In  it  the  water  is  at  a  temperature  of  one  hun- 
dred and  ten  degrees,  and  the  feet  are  immersed  for  five  or 
eight  minutes. 

Both  the  cold  and  hot  foot  bath  are  efficient  sleep-induc- 
ing agents  and  are  valuable  aids  for  the  relief  of  mental  irri- 
tability and  excitement,  and  of  the  disagreeable  subjective 
cerebral  sensations. 

The  Douche. — The  douche  excels  all  other  hydriatric 
measures  in  the  constitutional  treatment  of  neurasthenia  and 
hysteria.  Although  it  can  not  be  applied  during  the  rest 
cure,  it  is  a  seasonable  post-graduate  course  to  that  proced- 
ure, and  in  many  cases  of  functional  nervous  disease  of  mod- 
erate severity,  when  for  any  reason  the  rest  cure  is  not 
undertaken,  the  patients  recover  while  taking  cold  douches, 
without  their  ordinary  mode  of  hfe  being  seriously  inter- 
fered with.  For  the  successful  operation  of  this  form  of 
treatment  two  conditions  must  be  scrupulously  fulfilled. 
These  relate  to  temperature  and  pressure.  The  tempera- 
ture of  the  water  must  be  accurately  regulated  by  means  of 


4IO 


TREATMENT    OF    THE   TRAUMATIC   NEUROSES. 


the  thermometer,  in  order  that  the  patient  may  not  receive 
too  great  a  shock  from  the  water  being  too  cold,  or  that  he 
may  not  fail  to  react  quickly,  as  often  occurs  when  the  water 
is  too  warm.  The  force  with  which  the  douche  is  deliv- 
ered determines  the  degree  of  mechanical  irritation,  which 
is  nearly  as  important  a  factor  as  temperature.  A  douche, 
even  when  of  proper  temperature,  which  comes  to  the  pa- 
tient with  only  a  few  pounds  of  pressure  behind  it,  is  fol- 
lowed by  a  prompt  reaction  in  robust  persons  only ;  in  an 
anaemic  and  exhausted  individual  it  is  a  long  time  after  the 
contraction  caused  by  the  cold  before  the  capillaries  dilate 
again ;  the  desired  result  of  a  quick  alternation  of  vas- 
cular tone  is  consequently  not  obtained.  As  these  condi- 
tions are  difficult  of  fulfillment  in  private  houses,  it  is  desir- 
able for  the  patient  to  receive  this  treatment  in  institutions 
in  which  the  requirements  as  to  pressure  and  temperature 
can  be  obtained  and  the  physician's  directions  can  be  car- 
ried out  by  skilled  attendants.  The  treatment  should  be 
taken  every  day,  or  at  least  every  other  day.  The  ordinary 
method  in  hydriatric  establishments  is  for  the  patient  to  be 
placed  for  two  to  three  minutes  in  a  chamber  filled  with  hot 
air  (130°  to  150°).  On  emerging  he  immediately  gets  under 
a  rain  bath  of  sixty  to  seventy  degrees  of  temperature  and 
of  thirty  to  seventy  pounds  of  pressure.  The  degree  of  tem- 
perature and  the  amount  of  pressure  will  vary  according  to 
the  amount  of  stimulation  necessary  for  the  individual  case. 
The  colder  the  water,  and  the  greater  the  force  with  which 
it  strikes  the  body,  the  more  pronounced  is  the  effect.  The 
water  is  turned  off  at  the  end  of  one  or  at  most  two  min- 
utes ;  the  patient  is  then  quickly  dried  by  towels  and  by 
rubbing.  It  is  best  to  send  him  at  once  into  the  open  air, 
unless  he  be  very  feeble,  in  order  to  take  advantage  of  the 
deepened  inspirations  which  follow  the  douche.  As  the 
general  or  rain  douche  is  often  too  severe  at  the  beginning 
of  treatment,  a  way  may  be  pav^d  for  it  by  using  for  a  week 


HYDRIATRICS.  ^n 

or  two  the  spinal  fan  douche,  in  which  the  back  of  the  pa- 
tient is  pla3^ed  upon  by  water  coming  from  a  hose  fitted  with 
a  quarter-inch  nozzle,  the  stream  being  scattered  into  the 
shape  of  a  fan  by  placing  a  finger  upon  the  nozzle.  The  re- 
quirements as  to  temperature,  pressure,  and  duration  of  the 
rain  douche  and  the  spinal  douche  are  the  same.  Although 
the  spinal  douche  is  local  in  application,  its  effects  are  gen- 
eral. When  applied  to  other  circumscribed  areas,  this  form 
of  treatment  may  be  followed  by  improvement  in  local  symp- 
toms. It  often  acts  well  in  the  isolated  physical  manifesta- 
tions of  hysteria.  Under  the  local  cold  douche  of  twenty 
to  thirty-five  pounds  pressure  the  anassthesia,  paralysis,  or 
contracture,  when  of  functional  origin,  often  disappears. 
Local  and  general  douches  may  be  alternated. 

It  is  so  frequently  impossible  for  patients  needing  water 
treatment  to  have  access  to  properly  equipped  hydriatric  in- 
stitutions, that  it  is  often  necessary  for  them  to  get  along 
with  such  facilities  as  the  ordinary  dwelling  house  supplies. 
This  is  only  feasible,  however,  when  the  nervous  disease  has 
not  reached  a  high  degree  of  development.  When  the  pa- 
tient is  very  anaemic  or  very  much  exhausted  he  is  liable 
to  receive  more  harm  than  good  from  measures  which  can 
not  be  accurately  regulated  and  whose  effects  can  not  be 
carefully  observed.  The  cold  sheet,  the  foot  bath,  and 
packs  are,  of  course,  given  as  well  at  home  as  anywhere, 
provided  the  nurse  is  intelligent  and  skillful.  The  douche, 
however,  is  rarely  practicable  in  private  dwellings,  as  neither 
its  temperature  nor  its  force  can  be  properly  controlled. 
Still,  when  the  patient  is  reasonably  robust,  certain  substi- 
tutes for  it  are  possible.  These  are  the  ordinary  cold  shower 
bath,  provided  it  is  delivered  with  considerable  force ;  or 
the  full  cold  bath,  which  may  begin  with  the  water  at  eighty 
degrees,  a  temperature  which  is  gradually  lowered  ;  or,  if 
the  patients  react  well,  the  alternate  sponging  of  the  nape 
of  the  neck  and  spine  with  hot  (iio°)  and  cold  (65°)  water. 


412 


TREATMENT   OF    THE   TRAUMATIC   NEUROSES. 


The  local  douches  can  not  be  satisfactorily  carried  out  at 
home. 

Hypnotism. — If  hypnotism  is  understood  to  include 
every  variety  of  suggestion  by  which  the  mind  can  be  in- 
fluenced, it  is  a  procedure  which  will  never  be  eliminated 
from  the  practice  of  medicine.  The  effect  of  mental  prompt- 
ing is  evident  in  all  social  intercourse,  and  the  peculiar  re- 
lations existing  between  physician  and  patient  necessarily 
render  it  an  agent  of  great  power.  A  medical  man  is  sup- 
posed to  be  acquainted  with  the  solutions  of  all  the  prob- 
lems of  physiology,  and  the  patient  is  as  ready  to  believe 
what  the  physician  says  as  he  is  to  trust  to  his  own  sensa- 
tions. On  the  one  hand  is  a  person  whose  judgment,  will, 
and  self-control  have  been  weakened  by  illness  ;  on  the  other 
is  a  man  with  unimpaired  faculties,  conversant  with  human 
nature,  and  presumably  conversant  with  the  character  of  the 
symptoms  of  which  the  sufferer  complains.  Nothing  could 
be  more  natural  under  such  circumstances  than  that  the 
mental  actions  of  the  patient  be  to  a  certain  extent  directed 
and  controlled  by  those  of  the  more  vigorous  personality. 
In  general  diseases,  in  which  the  brain  is  apparently  unaf- 
fected, the  influence  of  mind  upon  body  is  too  far  reaching 
to  permit  of  neglect ;  and  in  the  functional  disorders  of  the 
nervous  system,  whose  symptoms  are  in  large  part  mental, 
the  patient  is  so  susceptible  to  the  appeals  to  the  emotions 
and  to  the  suggestions  or  counter-suggestions  of  certain 
trains  of  thought,  that  the  physician  who  neglects  these 
methods  can  hardly  hope  to  be  successful  in  his  treatment. 
Contrasted  with  this  form  of  suggestion,  which  every  phy- 
sician uses  almost  unconsciously,  is  that  which  is  made  dur- 
ing the  condition  of  induced  sleep. 

By  the  term  hypnosis  is  usually  understood  the  peculiar 
psychical  condition  brought  about  by  various  means,  during 
which  the  patient's  higher  consciousness  is  in  abej^ance.  In 
the  hypnotic  state  the  subject  may  be  made  to  do  things  of 


HYPNOTISM. 


413 


which  on  awakening  he  has  no  recollection  ;  also  sugges- 
tions made  during  this  state  may  be  subsequently  acted 
upon  independently  of  his  volition.  It  is  largely  by  means 
of  hypnosis  that  the  falsity  of  hysterical  symptoms  has  been 
shown. 

As  a  therapeutic  measure  it  has  been  generally  aban- 
doned by  the  school  of  the  Salpetriere.  It  is  still  used  in 
Germany,  but  its  special  European  exponents  are  Bernheim,^ 
of  Nancy  ;  Forel,  of  Zurich  ;  and  Wetterstrand,  of  Stock- 
holm. In  America  it  has  never  attained  popularity  among 
the  members  of  the  medical  profession,  partly  because  few 
American  physicians  have  had  the  opportunity  of  systemat- 
ically studying  its  modus  operandi  and  its  effects,  and  partly 
because  in  this  country  it  has  never  been  freed  from  the 
reputation  of  quackery.  Whatever  may  be  its  efficacy 
among  the  ignorant  peasantry  of  Europe,  in  this  country, 
whose  people  are  matter-of-fact  and  comparatively  free  from 
superstition,  the  therapeutic  uses  of  hypnotism  are  very  re- 
stricted. It  has  no  part  in  the  treatment  of  neurasthenia, 
and  in  hysteria  it  can  only  cause  a  disappearance  of  the 
individual  manifestations,  without  benefiting  the  funda- 
mental conditions  from  which  the  morbid  mental  states 
arise.  Even  did  we  not  accept  the  theory  of  Charcot,  that 
hypnotism  is  only  possible  in  the  victims  of  hysteria,  the 
ease  with  which  hysterical  persons,  who  have  once  been 
hypnotized  by  an  operator,  can  again  be  brought  under  this 
influence,  and  the  readiness  with  which  auto-hypnosis  comes 
to  take  an  important  place  among  hysterical  manifestations, 
are  sufficient  evidences  that  in  la  grande  nevrose  the  reaction 
to  suggesting  influences  occurs  more  readily  and  is  accom- 
panied by  more  permanent  effects  than  in  normal  individu- 
als. When  the  physician  succeeds  by  means  of  hypnosis  in 
causing  a  disappearance  of  any  of  the  physical  manifesta- 
tions of  hysteria,  he  does  so  by  bringing  about  an  alterna- 
tion of   personality,  during  which  the  subconscious  self  of 


414  TREATMENT   OF   THE    TRAUMATIC   NEUROSES. 

the  patient  receives  and  reacts  to  impressions  which  would 
not  affect  the  conscious  self  ;  but  since  the  nature  of  hyste- 
ria can  best  be  explained  by  assuming  that  the  physical 
manifestations  are  dependent  upon  alternations  of  person- 
ality and  upon  subconscious  mental  states,  it  would  seem  to 
be  an  unavoidable  conclusion  that  by  contributing  addi- 
tional phases  to  the  underlying  morbid  psychical  conditions 
the  whole  disorder  would  be  rendered  worse,  even  though 
the  temporary  physical  manifestations  are  made  to  disap- 
pear. Consequently  hypnotism  is  to  be  resorted  to  only 
when  other  therapeutic  means  have  proved  useless.  When 
the  patients  have  failed  to  receive  benefit  from  the  rest  cure, 
or  from  hydriatric  measures,  or  from  other  forms  of  treat- 
ment, hypnotic  suggestion  is  not  only  permissible,  but  re- 
mains as  the  one  therapeutic  measure  from  which  benefit 
may  be  hoped  for.  However,  as  Gilles  de  la  Tourette  says, 
"  Hypnotism  is  a  potent  modifier  of  hysterical  strata  and 
may  be  dangerous  even  in  skilled  hands.  It  should  only  be 
used  when  the  dangers  incurred  are  less  serious  than  the 
symptoms  which  it  is  intended  to  cure." 

Drugs. — The  use  of  drugs  in  the  treatment  of  the  neu- 
roses is  subsidiary  to  the  application  of  some  or  all  of  the 
procedures  which  have  been  described.  The  patients  are, 
however,  more  contented  if  they  are  taking  some  medicine, 
and  there  are  a  few  drugs  which  unquestionably  render  ma- 
terial assistance  in  the  treatment  of  these  conditions.  To 
combat  anaemia  and  for  purposes  of  general  nutrition,  some 
form  of  iron  or  arsenic  is  generally  useful.  When  the  gas- 
tric irritability  is  pronounced,  these  tonics  may  be  adminis- 
tered in  the  form  of  some  of  the  natural  waters,  such  as 
Levico,  which  contain  proportionately  large  amounts  of 
these  minerals.  The  most  popular  nerve  tonic  is  strychnine. 
It  may  be  given  by  mouth  in  the  form  of  the  sulphate, 
gr.  ^ig-  to  ^,  three  times  a  day  after  meals,  or  hypodermatic- 
ally,  as  the  nitrate,  gr.  ^.     Strychnine  is  to  be  especially 


DRUGS.  415 

recommended  when  the  clinical  manifestations  indicate  de- 
pression, rather  than  irritabihty,  of  the  nerve  centers.  A  new 
drug,  which  in  many  cases  yields  very  satisfactory  results,  is 
the  glycero-phosphate  of  soda.  It  may  be  prescribed  in 
three-  or  five-grain  capsules  (Chapoteau),  or  according  to  the 
following  formula: 

1^  Glycero-phosphate  of  soda  (Schering). ,    3vj; 

Distilled  water 5  viij. 

M.  Sig.  :  One  teaspoonful  in  hot  water,  three  times  a  day, 
half  an  hour  after  meals. 

The  bromides  may  do  a  great  deal  of  harm  in  neuras- 
thenia, and  their  indiscriminate  use  is  to  be  deprecated.  In 
small  doses  they  are  often  efficacious  in  allaying  extreme 
nervous  excitability,  especially  when  exhibited  in  conjunc- 
tion with  ergot.  They  may  also  be  recommended  for  the 
relief  of  dizziness  and  headache.  The  following  prescription 
has  proved  useful  in  the  hands  of  the  writer : 

jp,  Sodii  bromid 3  vj ; 

Ext.  ergot,  fl 5  j ; 

Aq.  destil q.  s.  ad    '^iv. 

M.  Sig. :  One  teaspoonful  in  hot  water  half  an  hour  after 
meals. 

Insomnia  can  usually  be  allayed  by  some  of  the  hydro- 
therapeutic  measures.  When  they  fail  to  induce  sleep,  re- 
course may  be  had  to  small  doses  of  the  bromides,  or  sul- 
phonal,  or  trional,  of  which  the  latter  is  the  most  efficient 
and  least  harmful.  Morphine  has  no  place  in  the  treatment 
of  the  traumatic  neuroses. 

For  constipation  much  can  be  done  by  massage,  although 
drugs  are  often  necessary.  A  teaspoonful  of  magnesium 
sulphate  in  a  full  glass  of  cold  water,  taken  on  rising  in  the 
morning,  is  in  many  cases  sufficient  to  insure  one  or  two 
movements  daily.  If  constipation  is  rebellious,  more  active 
measures  are  necessary.  When  possible,  the  natural  aperi- 
ent waters,  such  as  Hunyadi  or  Francis  Joseph,  are  pref- 


4i6 


TREATMENT   OF   THE   TRAUMATIC    NEUROSES. 


erable  to  other  laxatives.  The  fluid  extract  of  cascara, 
gtt.  X  to  XXX  once  or  twice  a  day,  or  at  bedtime,  gtt.  xlv, 
is  often  serviceable.  When  these  measures  fail,  recourse 
must  be  had  to  the  more  energetic  laxatives  or  purgatives, 
which  need  not  be  enumerated.  If  they  are  given  every 
night,  it  is  advisable  to  have  a  variety,  so  that,  by  taking  a 
different  one  each  night  in  the  week,  the  patient  does  not 
come  to  rely  too  much  on  any  one  of  them. 

Whatever  drugs  are  used,  they  should  be  given  for  defi- 
nite purposes,  and  should  be  taken  according  to  implicit 
directions.  Neurasthenic  patients  are  especially  fond  of 
dosing  themselves  on  the  appearance  of  every  new  symptom, 
and  of  accepting  as  genuine,  and  as  applicable  to  their  cases, 
the  cures  effected  under  this  or  that  specific  as  recorded  in 
the  advertising  columns  of  the  newspapers.  To  combat  this 
tendency  the  patient  should  be  told  the  nature  and  the  dose 
of  the  drugs  he  is  to  take,  and  when  he  is  to  take  them  ;  and 
he  should  be  particularly  cautioned  against  taking  anything 
in  the  way  of  medicines  without  the  physician's  orders. 

Such  are  the  most  important  of  the  measures  at  our  dis- 
posal for  the  treatment  of  the  traumatic  neuroses.  Varying 
conditions  may  occasionally  demand  additional  methods.  If 
the  suffering  from  lumbago  is  intense,  it  may  be  relieved  by 
the  application  of  a  plaster  jacket.  It  is  rarely  necessary  to 
continue  the  immobilization  for  more  than  a  week  or  ten 
days.  At  its  termination  the  muscles  of  the  back  should  be 
actively  massed.  The  cautery  is  often  used  in  this  condi- 
tion, since  it  alleviates  the  pain,  but  it  renders  the  back 
sensitive  and  postpones  the  possibility  of  massage.  Except 
in  so  far  as  it  supplies  exercise  for  the  muscles,  faradism  is 
of  but  little  service.  The  indefinite  pains  are  best  allayed 
by  rest  and  by  the  general  tonic  treatment.  If  true  neural- 
gia exists,  it  may  be  improved  by  hot  fomentations,  by 
some  of   the   analgesics,  by  the   application   of   galvanism. 


EXERCISE.  41-r 

or,  better,  by  ten-minute  daily  seances  with  the  sinusoidal 
current.  Also  the  vibrator,  as  devised  by  Peterson,  is  use- 
ful in  some  cases. 

Passive  movements  are  the  most  rational  means  for  caus- 
ing the  disappearance  of  hysterical  paralyses  and  contracture. 
By  causing  movement  in  limbs  which  are  apparently  para- 
lyzed, the  patient  sees  that  they  are  movable,  and  gradually 
comes,  when  sufficiently  encouraged,  to  move  them  himself. 
In  hysterical  paralysis  of  the  leg  the  power  of  walking  may 
often  be  speedily  restored  by  having  the  patient  push  a 
chair  in  front  of  him,  or  by  means  of  a  "  roller  machine." 
By  distracting  the  patient's  attention,  motion  can  usually  be 
obtained  in  hysterical  contractures,  and  gentle  and  persistent 
passive  movements  are  the  most  efficacious  means  of  treating 
this  condition.  By  massage,  also,  sensibility  may  be  made 
to  return  to  skin  which  was  the  seat  of  hysterical  anaesthesia. 
These  means,  the  beneficial  results  of  which  are  often  per- 
manent, are  much  to  be  preferred  to  those,  such  as  the  fara- 
dic  brush  or  the  horseshoe  magnet,  which  depend  for  their 
action  upon  fright,  or  upon  utilizing  the  credulity  of  the 
patient.  Some  general  exercise  should  be  insisted  upon  as 
soon  as  the  patient  is  able  to  undertake  it.  During  the 
rest  cure,  as  soon  as  complete  rest  is  abandoned,  the  patient 
should  be  made  to  perform  light  exercises,  such  as  opening 
and  closing  the  hands,  or  flexing  and  extending  the  elbows 
and  wrists,  as  a  part  of  the  daily  schedule.  Similarly,  he 
should  make  use  of  the  legs,  practising  getting  up  on  and 
down  from  a  chair,  and  walking  prescribed  distances  around 
the  room  at  regular  times.  For  the  rest-cure  patient,  as  he 
gets  better,  and  for  all  neurasthenic  and  hysterical  patients 
who  do  not  go  to  bed,  the  exercise  may  include  light  gym- 
nastics and  short  walks  or  drives,  but  may  be  gradually  ex- 
tended until  it  includes  some  of  the  moderate  athletic  sports 
for  which  the  facilities  are  now  becoming  so  generally  ac- 
cessible. 


4i8 


TREATMENT   OF   THE   TRAUMATIC   NEUROSES. 


Change  of  climate,  involving  as  it  does  diversion  of 
thought  and  modification  of  home  habits,  is  almost  always 
beneficial.  As  a  general  rule,  the  seashore  is  particularly- 
adapted  for  the  irritable  forms  of  disease,  while  patients  who 
are  depressed  and  apathetic  do  best  in  high  altitudes,  such 
as  may  be  found  in  Colorado  or  in  the  elevated  regions  of 
southern  California. 

Bibliography. 

Baruch,  Hydrotherapy.  Hare's  System  of  Therapeutics,  Phila- 
delphia, 1891. 

Bernheim,  Suggestive  Therapeutics.  Translated  by  Herter^ 
New  York,  1889. 

Forel,  Der  Hypnotismus.     Stuttgart,  1889. 

Mitchell,  Fat  and  Blood.     Philadelphia,  1891. 

Peterson,  Vibratory  Therapeutics.  Med.  News,  November^ 
1897. 

Wetterstrand,  Hypnotism.  Translated  by  Petersen,  New  York 
and  London,  1897. 

Winternitz,  Vortrage  iiber  Hydrotherapie. 


INDEX   OF   NAMES. 


Abercrombie,  187. 

Babinski,  323. 

Bailey,  95,  323,  392^ 

Ballet  and  Dutil,  i&b. 

Bannister,  140. 

Baruch,  406. 

Bass,  269. 

Beard,  227. 

Bechholm,  149. 

Berbez,  275,  279,  309. 

Bernhardt,  108,  163. 

Bernhardt  and  Kronthal,  336. 

Bernheim,  271,  413. 

Bikeles,  88. 

Binswanger,  140,  254,  256. 

Blocq,  300. 

Booth,  223. 

Bremer,  301,  357. 

Briquet,  272,  280. 

Brissaud,  273. 

Brodie,  272,  312. 

Bruns,  198. 

Bullard,  172. 

Carara,  122. 

Charcot,  62,  182,  210,  252,  270  ei  seq. 

Charcot,  J.  B  ,  165. 

Christian,  141. 

Clarke,  170,  189. 

Clevenger,  197. 

Comby,  317 

Craig,  163. 

Crocq,  199,  325. 


Dana,  29,  194,  199,  208,  275,  325,  326, 

358. 
Duchenne,  164. 

Eisenlohr,  171,  198. 
Erb,  115,  157,  159,  191. 
Erichsen,  3. 

Fischer,  87. 
Forel,  413. 
Forster,  221,  255. 
Fournier,  140. 
Fox,  149. 
Francotte,  318. 
Friedreich,  170. 

Godkin.  341,  358. 
Gowers,  87,  157,  181, 
Graefe,  von,  221. 
Gray,  130. 
Gudden,  140,  141. 
Guinon,  323. 

Hamilton,  138. 
Head,  90. 
Heller,  392. 
Hirsch,  166. 
Hirschl,  140,  141. 
Hitzig,  163. 
Hodge,  233. 
Hodges,  191. 
Hoedemaker,  115. 
Hoffman,  357. 
Howell  and  Huber,  118 


419 


420 


INDEX   OF    NAMES. 


Hughes,  211. 
Huisman,  124. 
Hun,  288. 

Interstate  Commerce  Commission,  204. 

Jacobson,  150. 
Janet,  286,  298. 
Jendrassik,  40. 
Judd,  358. 

Klumpke,  116. 

Knapp,  199,  209,  240,  259,  267,  275,  279, 

'^26.  367,  387.  388. 
K-Ocher,  90. 
Koenig,  221,  323. 
Krafft-Ebing,  142. 
Krauss,  38. 

Laehr,  124,  323. 

Lambret,  76. 

Laudun,  290. 

Lebrun,  303. 

Le  Grande  du  Saulle,  137. 

Lepois,  272. 

Levier,  78. 

Leyden,  8g. 

Litten,  106. 

Lloyd  and  Deaver,  129. 

Lugaro,  233. 

Mann,  172. 

Mannkopff,  219. 

Mason,  130. 

Mendell  and  Schnell,  140. 

Mendenhall,  7. 

Meyer,  142. 

Mickle,  147,  148. 

Minor,  80. 

Mitchell,  J.  K.,  118. 

Mitchell,  S.  W.,  118,  394. 

Miura,  303. 

Mobius,  271. 

Miiller,  221. 

Nammack,  266. 
Nonne,  329,  330. 


Oebeke,  140. 
Ollivier,  187. 
Oppenheim,  195,  196,  259,  262,  326,  333, 

334.  337- 
Outten,  199. 

Page,  192,  198,  230,  262,  321,  358,  366. 

Paget,  272. 

Parkin,  78. 

Peters,  221. 

Peterson,  11,  140,  294,418. 

Pettit,  14S. 

Pfeiffer,  96. 

Pitres,  313,  318,  379. 

Poncet,  170. 

Porcher,  210. 

Prentice,  341,  343,  352. 

Prince,  162,  299,  322,  352. 

Putnam,  194,  358. 

Quain,  iii. 

Raymond,  170. 
Regis,  140,  239. 
Reynolds,  273. 
Richer,  309,  314. 
Richter,  265. 
Riegler,  191,  357. 
Rumpf,  219. 

Saenger,  15,  199,  264,  337. 
Schlager,  141. 
Schmaus,  87. 
Schmidt-Rimpler,  393. 
Schultze,  198,  358. 
Schutte,  311. 
Schweigger,  24. 
Seeligmiiller,  358. 
Seguin,  558. 
Serieux,  306. 
Sherrington,  90. 
Smith,  344. 
Soukanoff,  159. 
Souques,  305. 

Sperling  and  Kronthal,  336. 
Starr,  90,  129,  132. 
Storbeck,  157. 


INDEX    OF    NAMES. 


421 


Strauss,  220. 
Stroebe,  118. 
Striimpell,  20,    123,   195, 

273- 
Sydenham,  272. 

Thomsen  and  Oppenheim, 
Thorburn,  77,  go. 
Tourette,  Gilles  de  la,  198, 

Unverricht,  124. 

Van  Deventer,  149. 

Vandier,  185. 

Van  Gehuchten,  53. 


199.   201,  222, 

194. 
305,  414- 


Van  Gieson,  78,  127. 
Vibert,  89,  228. 

Waldeyer,  54. 
Walton,  194,  203,  358. 
Walz,  184. 
Watson,  8g. 
Westphal,  igi. 
Westphal,  A..  86. 
Wetterstrand,  413. 
Wilbraud  and  Sanger,  255. 
Willard  and  Spiller,  86. 
Winternitz,  406. 

Zein,  322. 
I  Ziehen,  140,  172. 


28 


INDEX   OF   SUBJECTS. 


Abscess,  cerebral,  120. 
Aboulia,  hysterical,  2go. 
Accident  cases,  fraud  in,  347. 

frequency  of,  341. 
Accident,  history  of,  7. 
Acromegaly,  traumatic,  origin  of,  124. 
Alcoholism,  predisponent  to  nervous  dis- 
ease, 13. 

symptoms  of,  14. 
Amaurosis,  hysterical,  296. 
Amblyopia,  hysterical,  296. 
Amnesia  in  hysteria,  289. 
Amyosthenia,  301. 
Amyotrophic  lateral  sclerosis,  164. 
Anesthesia,  examination  for,  35. 

generalized,  218. 

glove,  293. 

in  brain  injuries,  60. 

in  hysteria,  291. 

in  locomotor  ataxia,  155. 

in  peripheral  nerve  injuries,  100. 

in  spinal-cord  injuries,  90. 

in  traumatic  neuroses,  218. 

in  the  unclassified  forms,  335. 
Anaesthesia,  general,  294, 
Anaesthesia,  total,  293. 

morphological,  293. 

segmental,  293. 

simulation  of,  378. 

stocking,  293. 
Analgesia,  in  hysteria,  292. 

in  spinal-cord  injuries,  80. 

in  simulation,  378. 

tests  for,  36. 
Angina  pectoris,  258. 


Ankle  clonus,  41. 

in  hysteria,  314. 

in  neurasthenia,  257. 

in  the  traumatic  neuroses,  222. 

in  the  unclassified  forms,  332. 

in  spinal-cord  injuries,  go. 
Anuria,  hysterical,  318. 
Aphasia,  52. 

Aphonia,  hysterical,  318. 
Apoplexy  and  head  injuries,  66. 

hysterical,  317. 
Argyll-Robertson  pupil,  23. 

in  general  paresis,  138. 

in  locomotor  ataxia,  154. 
Arterio-sclerosis,  as    a    predisponent   to 
nei"vous  disease,  16. 

pathological  significance  of,  336. 

symptoms  of,  17. 
Astasia-abasia,  300. 
Asthenopia  in  neurasthenia,  254. 
Ataxia,  in  hysteria,  307. 

locomotor,  151. 

tests  for,  36. 
Athetosis,  31. 
Atrophy,  myopathic,  164. 

of  optic  nerve,  160,  334. 

progressive  muscular,  164. 
Auditory  nerve,  injury  to,  59. 
Aura,  in  epilepsy  and  hysteria,  316. 
Auto-suggestion,  288. 

Back,  injuries  to  the,  244. 

Back  muscles,  spasm  of,  in  hysteria,  311. 

spasm  of,  in  traumatic  lumbago,  248. 
Barometer  of  hysteria,  298. 


422 


INDEX   OF   SUBJECTS. 


423 


Base  of  brain,  lesions  at,  57. 
Biceps  jerk,  37. 

Blepharospasm,  hysterical,  310. 
Boite  de  Flees,   386. 
Bone  conduction,  significance  of,  26. 
Brachial-plexus  palsy,  lower  arm  type  of, 
116. 

upper  arm  type  of,  115. 
Brain,  abscess  of,  120. 

centers  of,  51. 

concussion  of,  66. 

injuries  to,  46. 

railway,  186. 
Brown-Sequard  paralysis,  80. 
Bulbar  palsy,  171. 

Capsule,  lesions  of  internal,  57. 
Casque  neurasthenique,  252. 
Catalepsy,  290. 
Cerebellum,  injury  of,  60. 
Cerebro-spinal  axis,  52. 
Cervical  plexus,  injury  to,  106. 
Charcot  joints,  153. 
Chorea,  electric,  311. 
Circumflex  nerve,  injury  to,  107, 
Clavus  hystericus,  296. 
Claw  hand.     (See  Main  en  griffe.) 
Coggin's  stethoscope  test,  388. 
Coma,  48. 

hysterical,  316. 
Combined  palsies  of  the  upper  extremity, 

114. 
Concussion  of  the  brain,  66,  186. 

of  the  spinal  cord,  84,  186. 
Consciousness,  limitation  of,  286. 
Contracture,  hysterical,  308. 
Convulsive   attacks,    differential  diagno- 
sis of,  315. 

in  epilepsy,  131. 

in  hysteria,  315. 

simulation  of,  388. 
Corporeal  shock,  48. 
Cortical  lesions,  56. 
Coxalgia,  hysterical,  313. 
Cranial  nerves,  examination  of,  52. 

intracranial  lesions  of,  57. 
Creeping  palsy,  164. 
Cutaneous  reflexes,  37. 


Deaf-mutism,  hysterical,  318. 
Deafness,  simulated,  388. 
Death  in  hysteria,  318. 
Degeneration,  reaction  of,  44. 

stigmata  of,  12. 
Delirium,  in  head  injuries,  49. 

tremens,  15. 
Delusions,  of  grandeur,  145. 

in  alcoholism,  15. 
Dementia  after  cerebral  lesions,  119. 

epileptic,  134. 

in  the  unclassified  forms,  327. 

paralytica,  137. 
Diarrhoea,  nervous,  260. 
Diplopia,  23. 
Douche,  the,  409. 
Drip  sheet,  407. 
Dubini's  disease,  311. 
Dynamometer,  29. 
Dysarthria,  22. 

Electric   currents  as   causes   of  nervous 

disease,  207. 
Electrical  chorea,  311. 
Electrical  examination,  42. 
Epileptic  equivalents,  132. 

headache,  132. 

impulsions,  133. 
Epilepsy,  traumatic,  126. 

aetiology  of,  127. 

bibliography  of,  136. 

course  of,  134. 

diagnosis,  of,  134. 

frequency  of,  126. 

idiopathic,  126. 

Jacksonian,  126. 

pathology  of,  127. 

predisposition  to,  127,  128. 

symptoms  and  variations  of,  131,  132. 
Erb's  palsy,  115. 

points,  43. 
Erichsen's  disease,  197. 

theory  of  concussion,  189. 

views  on  spinal  injuries,  187. 
Exaggeration  of  symptoms  in  hysteria, 
285. 

in  malingering,  347. 

in  neurasthenia,  241,  265. 


424 


INDEX    OF    SUBJECTS. 


Examination  of  the  patient,  plan  of,  20. 
Eyes,  examination  of,  22. 

Face,  spasm  of,  311. 

Facial  nerve,  extra-cranial  injury  of,  103. 

intra-cranial  injury  of,  58. 
Facial  spasm  in  hysteria,  311. 
Fears  in  neurasthenia,  239. 
Fibrillation,  31. 
Field  of  vision,  examination  of,  24. 

in  hysteria,  297. 

in  locomotor  ataxia,  160. 

in  neurasthenia,  254. 

in  malingering,  387. 

in  the  traumatic  neuroses,  220. 

in  the  unclassified  forms,  334. 

significance  of,  limitation  of,  25. 
Fifth  nerve,  injury  of,  58. 
Foot  bath,  409. 

clonus,  41. 
Fourth  nerve,  injury  of,  58. 
Fractures  of  the  skull,  64. 

of  the  vertebrae,  72. 
Freeman  family,  history  of,  359. 
Frontal  lobes,  injury  to,  52. 
Functional  disease,  definition  of,  4. 

effects  of  injury,  186. 

Gait,  ataxic,  82. 

equine,  33. 

hemiplegic,  33. 

in  hysterical  paralysis,  302. 

in  neurasthenia,  243. 

in  paralysis  agitans,  179. 

in  traumatic  lumbago,  249. 

in  unclassified  forms,  329. 

of  motor  paralysis,  32. 

spastic,  33. 

types  of  in  nervous  disease,  32. 
General  paralysis  of  the  insane,  137. 
General  paresis;  aetiology  of,  139. 

and  syphilis,  139 

bibliography  of,  150. 

medico-legal  periods  of,  137. 

percentage  of  "  traumatic"  cases,  141, 

prodromal  stage,  137. 

proof  of  traumatic  origin,  146. 
Globus  hystericus,  318. 


Glosso-labio  laryngeal  paralysis,  171. 
Glycosuria,  222. 

Haematomyelia  and  syringomyelia,  79. 
disseminated,  82. 
with  injury  to  spinal  column,  74. 
without  injury  to  spinal  column,  77. 
Haematemesis,  222. 
HcEmatomyelopore,  78. 
Haematorrhachis,  with   injury  to   spinal 
column,  73. 
without  injury  to  spinal  column,  76. 
Haemoptysis,  222. 

Hallucinations,  after  head  injuries,  49. 
hysterical,  288. 
in  alcoholism,  15. 
Healing,  centers  of,  52. 

disturbances  of,  in  brain  injuries,  59. 
in  facial  palsy,  104. 
in  hysteria,  299. 
in  malingering,  388. 
in  neurasthenia,  256. 
in  the  unclassified  forms,  335. 
Heart,  palpitation   of,   in   neurasthenia, 

258. 
Hemianaesthesia,  hysterical,  293. 
in  brain  injuries,  61. 
symptomatic  significance  of,  62. 
Hemianopsia,  in  brain  injuries,  52,  57. 
Hemiplegia,  gait  of,  33. 
in  hysteria,  302. 
in  injuries  to  the  brain,  57. 
in  injuries  to  the  spinal  cord,  80. 
in  paralysis  agitans,  179. 
Haemorrhage,  of  the  brain,  63. 

of  the  spinal  cord,  73,  76. 
Heredity  and  nervous  disease,  6,  11. 
Hydriatrics,  405. 
Hydriatric  institutions,  406. 
Hypnotism  and  hysteria,  271. 

in  treatment  of  traumatic  neuroses,  412. 
Hypochondriasis  and  neurasthenia,  235. 
Hypoglossal  nerve,  injury  to,  105. 
Hysteria,  aetiology  of,  274. 
aboulia  in,  290. 
amnesia  in,  289. 
amyosthenia  in,  301. 
ancesthesia  in,  291. 


INDEX   OF    SUBJECTS. 


425 


Hysteria,  ataxia  in,  307. 

attacks  in,  315. 

barometer  of,  298. 

bibliography  of,  321. 

blepharospasm  in,  310. 

coma  in,  316. 

condition  of  sphincters  in,  315. 

contracture  in,  308. 

cough  in,  318. 

hallucinations  in,  288. 

hearing  in,  299. 

hiccough  in,  318. 

hemiplegia  in,  302. 

hypersesthesia  in,  295. 

joint  affections  in,  312. 

major,  270. 

mental  symptoms  in,  283. 

minor,  270. 

monoplegia  in,  303. 

motor  symptoms  in,  300. 

paraplegia  in,  305. 

paralysis  in,  300. 

pathology  of,  280. 

"  period  of  meditation  "  in,  300. 

polyplegia  in,  306. 

prognosis  of,  318. 

reflexes  in,  314. 

respiration  in,  318. 

smell  in,  299. 

special  senses  in,  296. 

symptoms  of,  280. 

taste  in,  299. 

traumatic,  270. 

tremors  in,  311. 

vision  in,  296. 
Hystero-epilepsy,  315. 
Hystero-genetic  zones,  295. 
Hystero-neurasthenia,  186. 

Injuries  to  the  back,  244. 
Injuries,  to  the  brain,  46. 

focal  symptoms  of,  49. 

general  symptoms  of,  47. 

in  the  cerebellum,  60. 

in  the  cortex,  56. 

in  the  internal  capsule,  57. 

in  the  pons,  57. 

in  the  tracts,  56. 


Injuries,  to  the  brain,  mental  symptoms 
of,  48. 

motor  symptoms  of,  52. 

prognosis  of,  120. 

reflexes  in,  62. 

sensory  symptoms  in,  60. 

speech  disturbances  in,  51. 

sphincters  in,  63. 

varieties  of,  63. 
Injuries  to  the  peripheral  nerves,  97. 

aetiology  of,  98. 

bibliography  of,  118. 

symptoms  of,  98. 

prognosis  of,  102. 
Injuries  to  nerves,  43. 
Injuries  to  the  spinal  cord,  aetiology  of,  70. 

bibliography  of,  95. 

causes  of,  70. 

classification  of,  71. 

prognosis  of,  121. 

symptoms  of,  90. 
Injury,  examination  for,  18. 

functional  effects  of,  186. 

history  of,  7. 

immediate  organic  effects  of,  46. 

ultimate  organic  effects  of,  119. 
Internal  capsule,  lesions  of,  57. 
Introduction,  i. 
Isolation,  397. 

Jacksonian  epilepsy,  126. 
Jendrassik  method  of  re-enforcing  knee- 
jerk,  40. 
Joints,  hysterical,  312. 

Klumpke's  palsy,  116. 
Knee-jerk  (see  also  Tendon  Reflexes), 
38. 

Lead  palsy,  differential  diagnosis  of,  167. 
Lightning,    cause    of    nervous    disease, 

210. 
Litigation  and  hysteria,  279. 

and  neurasthenia,  267. 

and  the  traumatic  neuroses,  214. 

frequency  of,  in  accident  cases,  341. 
Localization,  cerebral,  49. 
Local  spasms  in  hysteria,  310. 


426 


INDEX   OF   SUBJECTS. 


Locomotor  ataxia,  151. 

aetiology  of,  157. 

and  syphilis,  157. 

bibliography  of,  163. 

pre-ataxic  period  of,  157. 

proof  necessary  for  traumatic  origin  of, 
162. 

trauma  as  a  cause  of,  158. 
Lumbago,  traumatic,  244. 
Lumbar  plexus,  palsy  of,  117. 

Main  en   griffe,   in   ulnar   nerve    palsy, 
109. 

in  progressive  muscular  atrophy,  174. 
Magnetic  currents,  physiological  effects 

of,  295. 
Malingering,  341. 

bibliography  of,  392. 

inducement  to,  343. 

varieties  of,  347. 
Mania  after  head  injuries,  120. 
Mannkopff  test,  2ig. 

in  hysteria,  295. 

in  simulation,  384. 

in  traumatic  lumbago,  248. 
Massage,  399. 

Median  nerve,  injury  to,  107. 
Medulla,  injury  to,  60. 
Melancholia  after  head  injuries,  120. 
Memory  after  accidents,  21. 
Mental  state,  examination  of,  21. 
Meteorological  disturbances  as  causes  of 

nervous  disease,  210. 
Mind  blindness,  52. 

deafness,  52. 
Monoplegia  in  brain  injuries,  56. 

in  hysteria,  303. 

simulation  of,  376. 
Morbid  movements,  significance  of,  31. 
Motor  centers  of  brain,  53. 

points  of  Erb,  43. 

pathway,  description  of,  52. 
Multiple  cranial  nerve  injuries,  59. 
Multiple  sclerosis,   traumatic   origin  of, 

123,  338. 
Muscular  sense,  examination  of,  36. 

in  cortical  injuries,  56. 

in  hysteria,  307. 


Muscular  sense,  in  locomotor  ataxia,  157. 

atrophy,  progressive,  164. 

dystrophy,  progressive,  164. 
Musculo-cutaneous  nerve,  injury  to,  107. 
Musculo-spiral  nerve,  injury  to,  iii. 
Mutism,  hysterical,  318. 
Myelitis,  6B. 

Neck  muscles,  hysterical  spasm  of,  311. 
Nerves,  cranial,  52,  57. 

injuries  to,  97. 
Nervous  exhaustion,  226. 

prostration,  226. 

shock,  48. 
Neuralgia,  traumatic,  100. 

treatment  of,  416. 
Neurasthenia,  traumatic,  226. 

aetiology  of,  227. 

auditory  apparatus  in,  256. 

bibliography  of,  269. 

digestive  disturbances  of,  260. 

insanity  from,  265. 

mental  symptoms  of,  235. 

motor  symptoms  of,  242. 

ocular  symptoms  of,  254. 

prognosis  of,  261. 

reflexes  in,  256. 

sensory  symptoms  of,  244. 

smell  in,  256. 

symptoms  of,  234. 

taste  in,  256. 

treatment  of,  394. 

vascular  disturbances  of,  258. 
Neuritis,  ascending,  no. 

migrans,  no. 

traumatic,  97. 
Neuron,  description  of,  53. 
Neurons,  central  and  peripheral,  54. 

symptoms  of  injury  to,  55. 

Occipital  lobes,  injury  to,  52. 
Oculo-motor  nerves,  examination  of,  23. 
Olfactory  nerves,  injury  to,  57. 
Ophthalmoscope,  use  of,  23. 
Opisthotonos,  316. 

Oppenheim's  traumatic  neurosis,  ig6. 
Optic  nerve,  atrophy  of,  in  tabes,  160. 
atrophy  of,  in  unclassified  forms,  334. 


INDEX   OF   SUBJECTS. 


427 


Optic  nerve,  examination  of,  23. 

injury  of,  57. 
Optic  nerves,  injury  of,  57. 
Optic  neuritis  in  brain  injuries,  57. 
Optic  tracts,  injury  to,  57. 
Orbicularis  palpebrarum,  spasm  of,  310. 
Organic  effects  of  injury  to  the  nervous 

system,  46. 
Origin,  substitution  of,  352. 

Pain  and   hyperaesthesia,  simulation  of, 

383- 
Painful  points  in  hysteria,  295. 

in  neurasthenia,  244. 

in  traumatic  lumbago,  247, 
Pain  sensibility,  examination  of,  36. 
Palsy  (see  also  Paralysis). 

bulbar,  171. 

Bell's,  103. 

creeping,  164. 

facial,  103. 

shaking,  178. 
Parsesthesia  in  neurasthenia,  253. 
Paralysis  "as  a  fine  art,"  359. 

bulbar,  171. 

examination  for,  27. 

general,  137. 

in  brain  injuries,  52. 

in  hysteria,  306. 

in  peripheral-nerve  injuries,  99. 

in  spinal-cord  injuries,  90. 

in  the  unclassified  forms,  331. 

simulated,  373. 

types  of,  55. 
Paralysis  agitans,  178. 

aetiology  of,  180. 

anatomy  of,  178. 

bibliography  of,  185. 

course  of,  iSo. 

symptoms  of,  178. 

trauma  as  cause  of,  182. 
Paramyoclonus  multiplex,  311. 
Paraplegia,  hysterical,  305. 

in  spinal-cord  injuries,  90. 

simulated,  375. 
Parkinson's  disease,  178. 
Patient,  examination  of,  6. 

general  appearance  of,  20. 


Patient,  previous  history  of,  6. 
Perimeter,  use  of,  24. 
"  Period  of  meditation,"  300. 
Peripheral  nerves,  injuries  to,  97. 
Petit  mal,  132. 
Physical  shock,  48. 
Plessimeter,  38. 
Polyopia,  299. 
Pontine  lesions,  57. 

Posterior  thoracic  nerve,  injury  to,  106. 
Predisposition  to  nervous  disease  in  epi- 
lepsy, 127. 

in  general  paresis,  139. 

in  hysteria,  274. 

in  locomotor  ataxia,  157. 

in  neurasthenia,  228. 

in  paralysis  agitans,  178. 

in  progressive  muscular  atrophy,  166. 

in  the  traumatic  neuroses,  211. 

physical  evidences  of,  11. 
Progressive  muscular  atrophy,  164. 

aetiology  of,  166. 

anatomy  of,  164. 

bibliography  of,  177. 

course  of,  166. 

illustrative  cases  of,  169. 

symptoms  of,  165. 

trauma  as  a  cause  of,  167. 
Psychoses  after  head  injuries,  120. 
Ptosis,  58. 

apparent  in  hysteria,  310. 
Pupil,  Argyll-Robertson,  23. 

examination  of,  22. 
in  epilepsy,  316. 

state  of,  in  general  paresis,  138. 
in  hysteria,  296. 
in  locomotor  ataxia,  154. 
in  neurasthenia,  254. 

Railway  accidents,  U.  S.  statistics  of,  204. 

as  causes  of  nervous  disease,  204. 
Railway  injuries,  statistics  concerning,  8. 
Railway  spine,  186. 

brain,  186. 
Reaction  of  degeneration,  44. 
Reflex,  abdominal,  37. 

cilio-spinal,  37. 

cremaster,  37. 


428 


INDEX   OF    SUBJECTS. 


Reflex,  patella,  38. 

plantar,  37. 
Reflexes  (see  also  Tendon  Reflexes). 

superficial,  37. 

deep,  38. 

tendon,  38. 

pupillary,  22. 

examination  of,  37. 

pharyngeal,  37. 
Rest  cure,  The,  395. 
Rigidity,  significance  of,  301 
Rohrenbildung,  78. 
Romberg  symptom,  34. 

in  locomotor  ataxia,  154 
Rhythmical  chorea,  311. 

Sacral  plexus,  palsy  of,  117. 

Saturday-night  paralysis,  99. 

Scoliosis,  hysterical,  31 1. 

Section  of  nerves,  103. 

Seismic  phenomena,  as  causes  of  nervous 

disease,  210. 
Sensation,  examination  of,  34. 
Seventh    nerve,    extracranial    injury    to, 
103. 

intracranial  injury  to,  58. 
Shaking  palsy,  178. 
"  Shifting  type  of  contraction  "  of  visual 

fields,  255. 
Shock,  nervous,  48. 

physical,  48. 
Sight,  centers  of,  52. 
Simulation,  357. 

bibliography  of,  392. 

detection  of,  369. 

difficulties  of,  363. 

frequency  of,  357. 

of  anaesthesia,  378. 

of  convulsive  attacks,  388. 

of  deafness,  388. 

of  individual  symptoms,  373. 

of  ocular  symptoms,  384. 

of  pain  and  hypersesthesia,  383. 

of  paralysis,  373. 

of  reflexes,  391. 

of  tremor,  377. 

of  vascular  disturbances,  389. 
Sixth  nerve,  injury  of,  58. 


Slowed  conduction,  36. 
Smell,  examination  of,  22, 
Somnambulism,  133,  2go. 
Spasmodic  twitchings,  31. 
Speculation  in  damage  claims,  345. 
Speech,  centers  of,  52. 

disturbances  of,  in  brain  injuries,  51. 

in  general  paresis,  138. 

in  hysteria,  318. 

in  neurasthenia,  240. 

in  the  unclassified  forms,  331. 
Sphincters,  condition  of,  in  brain  injuries, 

63- 

in  hysteria,  315. 

in  simulation,  390. 

in  spinal-cord  injuries,  90. 

in  traumatic  lumbago,  250. 
Spinal  ansemia,  186. 
Spinal  cord,  injuries  to,  68. 

protection  of,  69. 

concussion  of,  84. 

commotion  of,  84. 
Spine,  concussion  of,  186. 

injury  to,  244. 

railway,  186. 
Sponge  bath,  407. 
Spinal  irritation,  186,  194. 
Stepping  gait,  34. 
Stigmata  of  degeneration,  12. 

of  hysteria,  280. 
Stupor,  48. 

Subconsciousness,  286. 
Substitution  of  origin,  352. 

in  the   chronic  degenerative  diseases, 

354- 

in  the  traumatic  neuroses,  356. 
Suggestibility  in  hysteria,  287. 
Suicide  in  neurasthenia,  238. 

in  the  unclassified  forms,  339. 
Syphilis  as   a   predisponent    to   nervous 
disease,  15. 

and  tabes,  157. 

and  general  paresis,  139. 
Syringomyelia,  and  h^matomyelia,  79. 

traumatic  origin  of  124. 

Tabes  dorsalis,  151. 
Tachycardia,  significance  of,  217. 


INDEX    OF    SUBJECTS. 


429 


Tachycardia,  in  alcoholism,  14. 
in  malingering,  3S9. 
in  neurasthenia,  258. 
Taste,  examination  of,  26. 
Temperature  sense,  examination  of,  36. 
Temporal  lobes,  injury  to,  52. 
Tendon  reflexes,  diagnostic  value  of,  38, 
222. 
examination  of,  38. 
in  brain  injuries,  62. 
in  general  paresis,  138. 
in  hysteria,  315. 
in  locomotor  ataxia,  154. 
in  malingering,  391. 
in  neurasthenia,  257. 
in  peripheral-nerve  injuries,  lOi. 
in  spinal-cord  injuries,  90. 
in  the  traumatic  neuroses,  222. 
in  the  unclassified  forms,  232. 
in  traumatic  lumbago,  250. 
Thermo-ansesthesia  in  hysteria,  292. 
in  spinal-cord  injuries,  80. 
in  simulation,  380. 
tests  for,  36. 
Third  nerve,  injury  of,  57. 
Tongue,  hysterical  spasm  of,  311. 
Torticollis,  hysterical,  311. 
Touch,  examination  of,  36. 
Tract,  lesions  of  brain,  56. 
Tracts,  cerebro-spinal,  of  motion,  53. 
Traumatic,  definition  of,  i. 
Traumatic  hysteria,  270. 
Traumatic  lumbago,  244. 
duration  of,  251. 
Mannkopff  test  in,  248. 
symptoms  of,  246. 
Traumatic  neurasthenia,  226. 
Traumatic  neuroses,  186. 
aetiology  of,  203. 
anaesthesia  in,  218. 
bibliography  of,  223. 
cardiac  symptoms  in,  217. 
classification  of,  201. 
electricity  as  a  cause  of,  207. 
glycosuria  in,  222. 
history  of,  186. 
lightning  as  a  cause  of,  2TO. 
litigation  as  a  causal  factor,  215. 


Traumatic  neuroses,  meteorological  dis- 
turbances as  a  cause  of,  210. 

nomenclature  of,  200. 

occupation  as  a  causal  factoi",  212. 

pain  and  hypersesthesia  in,  219. 

pathology  of,  202. 

physical  condition  as  a  causal  factor, 
213. 

predisposition  as  a  causal  factor,  211. 

suggestion    by  physicians  as  a  causal 
factor,  213. 

symptoms  of,  215. 

tendon  reflexes  in,  222. 

treatment  of,  394. 

unclassified  forms  of,  325. 

visual  disturbances  in,  220. 

vomiting  in,  222. 
The  traumatic  neurosis,  186,  ig6. 
Traumatic  suggestion,  273,  300. 
Treatment  of  traumatic  neuroses,  394. 

bibliography  of,  418. 

climate  in,  418. 

diet  in,  400. 

drugs  in,  414. 

electricity  in,  400. 

exercise  in,  417. 

general  management  in,  402. 

hydriatrics  in,  405. 

hypnotism  in,  412. 

isolation  in,  397. 

massage  in,  399. 

rest  cure  in,  395. 

rest  in  bed  in,  398, 

vibrator  in,  417. 
Tremor,  31. 

alcoholic,  14. 

of  general  paresis,  138. 

of  multiple  sclerosis,  123. 

in  the  unclassified  forms,  328. 

of  paralysis  agitans,  178. 

hysterical,  311. 

neurasthenic,  243. 

simulated,  377. 
Triceps-jerk,  38. 
Trophic    disturbances,   examination  for, 

41. 
Tumors    of    nervous    system,    traumatic 
origin  of,  121. 


430 


INDEX    OF    SUBJECTS. 


Ulnar  nerve,  injury  to,  io8. 

Ultimate  organic  effects  of  injury,  iig. 

Unclassified  forms  of  traumatic  neuroses, 

325- 
setiology  of,  326. 
bibliography  of,  340. 
deep  reflexes  in,  332. 
diagnosis  of,  237. 
disturbances  of  motion  in,  328. 
general  symptoms  of,  335. 
hearing  in,  335. 
mental  symptoms  of,  327. 
optic  atrophy  in,  334. 
pathology  of,  336. 
prognosis  of,  337. 
sensory  symptoms  in,  332. 
special  senses  in,  335. 


Unclassified  forms  of  traumatic  neuroses, 
symptoms  of,  327. 
taste  and  smell  in,  335. 
vision  in,  334. 
Upper   extremity,  combined   palsies   of, 
114. 


Vascular     disturbances,    simulation 

389- 
Vertebrae,  fractures  of,  72. 
Vision,  examination  of,  22. 
Vision,  field  of,  25. 

Wet  pack,  408. 
"Winged  scapulae,  107. 
Wrist-drop,  99. 
Wryneck,  hysterical,  311, 


of. 


THE   END. 


A  TREATISE  ON 

THE  DISEASES   OF  THE 

NERVOUS   SYSTEM. 

By  WILLIAM  A.  HAMMOND,  M.  D., 

Surgeon-General  U.  S.  Army  (retired  list). 

With  the   Collaboration  of  GRAEME  M.  HAMMOND,  M.  D., 

Professor  of  Diseases  of  the  Mind  and  Nervous  System  in  the  New  York 
Post-Graduate  Medical  School  and  Hospital,  etc. 

With  118  Illustrations. 
NINTH    EDITION,    WITH    CORRECTIONS    AND    ADDITIONS. 


8vo.    932  pages.    Cloth,  $5.00;  sheep,  $6.00. 


"  Dr.  Hammond's  treatise  on  the  diseases  of  the  nervous  system  is  a  work  which 
has  been  long  familiar  to  the  profession,  and  has  attained  a  great  reputation  among 
the  standard  books  for  reference.  In  the  preparation  of  the  present  edition  the 
author  has  been  aided  by  his  son.  A  vast  amount  of  clinical  material  is  made  use 
of,  and  the  results  of  experimental  investigation  recorded.  The  book  is  written  in 
a  clear  and  pleasing  style,  and  obscure  conditions  are  dealt  with  in  a  manner  which 
will  prove  of  great  assistance  in  the  study  of  this  most  interesting  class  of  diseases." 
— Canadian  Practitioner. 

"  Dr.  Hammond  published  the  first  edition  of  his  '  Treatise  on  Diseases  of  the 
Nervous  System '  in  1871.  It  has  therefore  been  before  the  profession  for  twenty 
years,  and  during  these  years  it  has  continued  to  grow  in  public  favor,  this  being 
the  ninth  edition  that  has  been  issued.  Appreciation  of  this  work  has  not  only 
been  shown  in  this  country,  but  abroad,  as  it  has  been  translated  into  the  French, 
the  Italian,  and  the  Spanish  languages.  The  present  edition  has  been  thoroughly 
revised,  and  several  new  chapters  added.  This  is  a  book  of  such  great  value,  and  is 
referred  to  so  frequently  by  the  medical  press  and  other  medical  works,  that  no 
library  is  complete  without  it." — Alabama  Medical  and  Surgical  Age. 

"  There  are  few  books,  even  upon  those  subjects  which  are  constantly  in  the 
ordinary  physician's  mind,  which  succeed  as  has  that  of  Dr.  Hammond  ;  and  when 
we  recollect  that  when  the  first  edition  of  this  work  appeared,  neurology  in  America 
was  in  its  very  infancy,  the  rapid  exhaustion  of  its  editions  is  the  more  remarkable. 
In  the  ninth  edition  the  writer's  son  has  done  much  toward  keeping  the  work  abreast 
of  the  times,  and,  with  more  confidence  than  ever,  it  can  now  be  regarded  as  one  of 
the  best  and  most  satisfactory  works  on  nervous  diseases,  either  for  the  practitioner 
or  for  the  advanced  student.  The  book  is  beautified  and  its  usefulness  increased  by 
a  larger  number  of  illustrations  than  heretofore — among  the  best  from  a  medical 
point  of  view  being  those  representing  syringo-myelia,  which  have  been  taken  from 
the  studies  of  Van  Giesen." — Medical  Netcfi. 


D.   APPLETON    AND   COMPANY,  NEW    YORK. 


THE    DISEASES    OF 
THE   NERVOUS    SYSTEM. 

a  text-book  for  physicians  and  students. 
By    De.    LUDWIG    HIRT, 

PEOFESSOE  AT  THE  UNIVEESITT  OF  BEESLAU. 

second  amebican  edition,  revised  from  the  second  german  edition 
By  august   HOCH,   M.  D., 

ASSISTED  BY 

FRANK  R.    SMITH,   A.  M.    (Cantab.),  M.  D., 

ASSISTANT  PHTSICIAUS   TO   THE   JOHNS   HOPKINS   HOSPITAL. 

WITH  AN  INTRODUCTION 
By  WILLIAM  OSLER,  M.  D.,   F.  R.  C.  P., 

PEOFESSOE   OF  MEDICINE  EN   THE  JOHNS   HOPKINS  UNIVEESITT,   AND   PHYSICIAN  IN  CHIEF  TO  THB 
JOHNS  HOPKINS   HOSPITAL,   BALTLMOEE. 

8vo,  715  pages.     "With  181  Illustrations. 
Cloth,  $5.00;   sheep,  $6.00. 


"  This  work  possesses  many  points  -which  are  sufficiently  novel  to  justify  its  transla- 
tion and  publication  in  this  country.  The  general  practitioner  is  perhaps  more  in  need 
of  reliable  text-books  on  diseases  of  the  nervous  system  than  is  the  specialist.  .  .  .  The 
volume  before  us  admirably  meets  his  requirements,  and  to  a  very  great  extent  covers 
those  parts  of  the  study  which  have  not  been  fully  presented  by  former  writers.  .  .  . 
The  work  of  the  translators  is  perfect,  leaving  no  trace  of  the  German  idioms." — Ohio 
Medical  Journal. 

"  The  profession  of  this  country  stands  under  the  greatest  obligation  to  the  trans- 
lators of  this  standard  work  for  having  thus  furnished  the  opportunity  of  making  use  of 
one  of  the  best  works  ever  published  upon  the  subject.  As  a  work  of  reference  to  the 
physician  it  has  no  equal.  To  specialists  in  this  branch  of  diseases  it  is  invaluable.  As 
features  of  especial  commendation  may  be  mentioned  the  author's  clearness  in  the  ana- 
tomical and  symptomatological  arrangement  of  diseases." — Nashville  Journal  of  JiJedicine 
and  Surgery. 

"  The  translators  of  this  volume  have  conferred  a  favor  upon  English-reading  mem- 
bers of  the  profession  by  their  excellent  rendering  of  the  work  of  Professor  Hirt.  The 
text  is  especially  valuable  for  the  clear,  accurate,  and  well-ordered  description  of 
pathological  anatomy  and  symptomatology.  As  regards  treatment,  the  author  may  be 
accepted  as  a  safe  guide.  .  .  .  The  typography  and  plates  of  this  work  are  all  that  can 
be  desired." — Medical  Bulletin. 


D.   APPLETON   AND    COMPANY,  NEW  YORK, 


A  New,  Thoroughly  Revised,  and  Enlarged  Edition  of 

QUAIN'S 
DICTIONARY  OF  MEDICINE. 

BY   VARIOUS   WRITERS. 

Edited  by  Sir  RICHARD   QUAIN,   Bart.,  M.  D.,  LL.  D.,  etc., 

Physician  Extraordinary  to  Her  Majesty  the  Queen  ;  Consuhing  Physician  to  the   Hospital  for  Diseases 

of  the  Chest,  Brompton,  etc. 

Assisted  by  FREDERICK   THOMAS    ROBERTS,   M.  D.,  B.  Sc, 
Fellow  of  the  Royal  College  of  Physicians,  etc. ; 

And  J.   MITCHELL   BRUCE,  M.A.,  M.  D., 
Fellow  of  the  Royal  College  of  Physicians,  etc. 

With  an  American  Appendix  by  SAMUEL  TREAT  ARMSTRONG,   Ph.D.,  M.  D., 

Visiting  Physician  to  the  Harlem,  Willard  Parker,  and  Riverside  Hospitals,  New  York. 


IN   TWO   VOLUMES.  Sold  only  by  subscription. 


This  work  is  primarily  a  Dictionary  of  Medicine,  in  which  the  several  diseases  are  fully 
discussed  in  alphabetical  order.  The  description  of  each  includes  an  account  of  its  etiology 
and  anatomical  characters ;  its  symptoms,  course,  duration,  and  termination  ;  its  diagnosis, 
prognosis,  and,  lastly,  its  treatment.  General  Pathology  comprehends  articles  on  the  origin, 
characters,  and  nature  of  disease. 

General  Therapeutics  includes  articles  on  the  several  classes  of  remedies,  their  modes  of 
action,  and  on  the  methods  of  their  use.  The  articles  devoted  to  the  subject  of  Hygiene  treat 
of  the  causes  and  prevention  of  disease,  of  the  agencies  and  laws  affecting  public  health,  of 
the  means  of  preserving  the  health  of  the  individual,  of  the  construction  and  management  of 
hospitals,  and  of  the  nursing  of  the  sick. 

Lastly,  the  diseases  peculiar  to  women  and  children  are  discussed  under  their  respective 
headings,  both  in  aggregate  and  in  detail. 

The  American  Appendix  gives  more  definite  information  regarding  American  Mineral 
Springs,  and  adds  one  or  two  articles  on  particularly  American  topics,  besides  introducing 
some  recent  medical  terms  and  a  few  cross-references. 

The  British  Medical  Jour7ial  says  of  the  new  edition  : 

' '  The  original  purpose  which  actuated  the  preparation  of  the  original  edition  was,  to 
quote  the  words  of  the  preface  which  the  editor  has  written  for  the  new  edition,  '  a  desire  to 
place  in  the  hands  of  the  practitioner,  the  teacher,  and  the  student  a  means  of  ready  reference 
to  the  accumulated  knowledge  which  we  possessed  of  scientific  and  practical  medicine,  rapid 
as  was  its  progress,  and  difficult  of  access  as  were  its  scattered  records.'  The  scheme  of  the 
work  was  so  comprehensive,  the  selection  of  writers  so  judicious,  that  this  end  was  attained 
more  completely  than  the  most  sanguine  expectations  of  the  able  editor  and  his  assistants 
could  have  anticipated.  ...  In  preparing  a  new  edition  the  fact  had  to  be  faced  that  never 
in  the  history  of  medicine  had  progress  been  so  rapid  as  in  the  last  twelve  years.  New  facts 
have  been  ascertained,  and  new  ways  of  looking  at  old  facts  have  come  to  be  recognized  as 
true.  .  .  .  The  revision  which  the  work  has  undergone  has  been  of  the  most  thorough  and 
judicious  character.  .  .  .  The  list  of  new  writers  numbers  fifty,  and  among  them  are  to  be 
found  the  names  of  those  who  are  leading  authorities  upon  the  subjects  which  have  beea 
committed  to  their  care." 


D.   APPLETON    AND    COMPANY,    NEW   YORK. 


THE 

SCIENCE  AND  AET  OF 
MIDWIFERY. 

By  WILLIAM  THOMPSON  LUSK,  M.  A.,  M.  D., 

Professor  of  Obstetrics  and  Diseases  of  Women  and  Children  in  the  Bellevue 
Hospital  Medical  College ;  Obstetric  Surgeon  to  the  Maternity       , 
and  Emergency  Hospitals  ;  and  Grynaecologist 
to  the  Bellevue  Hospital. 


FOURTH   EDITION.     REVISED  AND   REWRITTEN. 
With  246  Illustrations. 

8vo.    Cloth,  $5.00 ;  sheep,  $6.00. 


"  It  was  the  pleasure  of  the  undersigned  to  write  a  review  of  this  most 
excellent  and  masterly  work  on  obstetrics,  when  it  appeared  in  its  first 
edition.  The  present  is  the  fourth,  an  edition  enlarged  and  revised.  It  is 
a  model  of  recent  medical  literature  in  obstetrics,  and  can  not  but  give 
great  credit  to  the  author  and  to  American  medicine.  Model  it  is  of  clear, 
forcible,  and  beautiful  English,  of  good  arrangement  of  subject-matter,  and 
of  thoroughness  of  modern  obstetric  exposition.  The  changes  which  have 
taken  place  in  the  theory  and  practice  of  obstetrics  since  the  issue  of  the 
last  edition  have  made  it  necessary  for  the  author  to  present  to  the  pro- 
fession what  is  essentially  a  new  book.  Most  cheerfully  will  we  recommend 
to  the  students  of  medicine  a  study  of  Lusk.  It  ranks  well  with  Playfair, 
and  is  second  to  no  book  in  our  language." — Chauncey  D.  Palmer,  in  the 
Ohio  Medical  Journal. 

"  The  book  is  now  beyond  criticism,  for  it  has  been  accepted  by  the  un- 
erring judgment  of  the  great  body  of  physicians.  We  congratulate  Dr. 
Lusk  upon  this  reward  for  the  immense  labor  he  has  bestowed  upon  it." — 
New  York  Medical  Journal. 

"It  contains  one  of  the  best  expositions  of  the  obstetric  science  and 
practice  of  the  day  with  which  we  are  acquainted.  Throughout  the  work 
the  author  shows  an  intimate  acquaintance  with  the  literature  of  obstet- 
rics, and  gives  evidence  of  large  practical  experience,  great  discrimination, 
and  sound  judgment.  We  heartily  recommend  the  book  as  a  full  and  clear 
exposition  of  obstetric  science,  and  safe  guide  to  student  and  practitioner." 
— London  Lancet. 

"  It  is  but  a  short  time  since  we  had  occasion  to  review  this  work,  of 
which  we  were  enabled  to  speak  in  the  highest  terms  of  praise.  The  rapid 
advance  of  many  departments  of  obstetrics  has  meantime  called  for  a  few 
additions.  These  having  been  made,  it  can  be  confidently  said  that  Lusk's 
Midwifery  holds  a  high  place  among  American  authors,  and  deserves  to 
be  extensively  employed  for  reference,  and  recommended  to  students  as 
a  reliable  and  unusually  readable  text-book." — Canada  Medical  and 
Surgical  Journal. 


D.   APPLETON    AND    COMPANY,  NEW    YORK. 


THE   PRINCIPLES   AND   PRACTICE 
OF    MEDICINE. 

By  WILLIAM   OSLER,    M.  D., 

Fellow  of  the  Royal  College  of  Physicians,  London ;   Professor  of  Medicine  in  the  Johns  Hopkins  Univer- 
sity, and  Physician  in  Chief  of  the  Johns  Hopkins  Hospital,  Baltimore;  formerly  Professor  of 
the  Institutes  of  Medicine,  McGill  University,  Montreal;  and  Professor  of  Clinical 
Medicine  in  the  University  of  Pennsylvania,  Philadelphia. 


THE    WORK   HAS   BEEN   REWRITTEN,    ENLARGED,    ENTIRELY   RESET^ 
AND  BROUGHT   UP   TO  DATE  IN  ALL  DEPARTMENTS. 


THIRD    EDITION. 
SOLD    ONLY     BY     SUBSCRIPTION. 


8vo,  1181  pages.      Cloth,  $5.50;    sheep,  $6.50;   half  morocco,  $7.00. 


"  With  new  type,  clear  paper  of  the  best  quahty,  and  a  somewhat  enlarged  page,  necessi- 
tated by  the  amount  of  matter  in  the  very  thorough  revision  of  a  book  whose  first  edition 
appeared  six  years  ago,  Osier's  Practice  comes  to  us  with  that  handsome  entowage  its  prime 
excellence,  merit,  and  true  value  demand.  .  .  .  From  first  to  last,  title-page  to  index,  the 
work  is  thoroughly  practical,  and  as  a  guide  in  diagnosis,  symptomatology,  and  treatment, 
will  be  found  well-nigh  incomparable,  and  can  not  but  be  the  more  appreciated  the  more  its 
sound  advice  and  wise  counsel  are  sought,  whether  by  the  neophyte  in  medicine  or  the  most 
experienced  clinician." — Sout/ier?i  Practitioner . 

"  We  have  little  to  add  to  our  notice  of  the  second  edition  {vide  Journal,  November  30, 
1895,  page  966).  The  criticisms  then  made  hold  good  now,  but  we  regarded  the  work  as  one 
of  the  ablest  contributions  to  the  literature  of  the  subject  in  this  country,  an  opinion  which 
we  still  hold." — Journal  of  the  American  Medical  Association. 

"  The  first  edition  was  great,  the  second  greater,  and  this  last  greatest  of  dW'—Cittcin- 
nati  Lancet-Clinic. 

"  There  are  few  books  which  receive  professional  confidence  and  esteem  to  the  extent  of 
that  received  by  Dr.  Osier's  well-known  work,  for  three  large  editions  have  been  presented  to 
us  in  a  period  of  about  six  years." — Theraj>eutic  Gazette. 

"  The  work,  like  former  editions,  is  thoroughly  practical  in  its  character,  fully  up  with  the 
times  and  down  to  date,  and  is  a  safe  guide  to  all  practitioners  who  may  consult  its  pages. 
The  student  of  medicine,  whose  time  is  so  much  occupied  by  the  tremendous  amount  of 
knowledge  he  is  expected  to  master  before  graduation,  will  find  here  exhaustiveness  without 
verbosity  and  a  plain  matter-of-fact  method  of  discussing  the  characters  of  different  diseases,, 
that  can  not  fail  to  instruct  without  wearying." — Journal  of  Medicine  and  Science. 


D.  APPLETON  AND  COMPANY,  NEW  YORK. 


j; 

A  SYSTEM  OF 

GENITO-URINARY  DISEASES, 

SYPHILOLOGY,  and  DEMATOLOGY. 

CONSISTING  OF  THREE  VOLUMES,  AS  FOLLOWS: 

Vol.  I,  GENITO-URINARY  DISEASES;  Vol.  II,   SYPHILOLOGY; 
and  Vol.  Ill,    DERMATOLOGY. 

BY  VAEIOirS  AUTHORS. 
Edited  by  PRINCE   A.  MORROW,  M.  D. 

SOLD    ONI.Y    BY    SUBSCRIPTION. 

"  Volume  I,  Genito-Urinary  Diseases. — The  first  of  these  three  volumes,  which 
has  recently  appeared,  gives  ample  evidence  of  the  liberality  and  thorough  work- 
manship of  its  publishers,  and  of  care  and  thought  on  the  part  of  its  editor,  to 
whom  great  credit  is  due  for  the  admirable  manner  in  which  he  has  accomplished 
the  arduous  task  involved  in  the  preparation  and  production  of  such  an  important 
work  as  this  is.  .  .  ,  Of  the  work  as  a  whole,  we  do  not  hesitate  to  say  that  it  is 
the  most  complete  and  best  single  publication  of  all  those  which  profess  to 
cover  the  ground  of  genito-urinary  diseases,  with  which  we  are  acquainted,  and 
recommend  it  cordially  to  the  favorable  consideration  of  the  profession." — Boston 
Medical  and  Surgical  Journal. 

"  The  second  volume  of  this  valuable  series  is  before  us.  It  covers  fully  the 
field  of  Syphilography,  and  is  in  itself  a  complete  text-book  of  nine  hundred  royal 
octavo  pages.  The  editor,  with  the  aid  of  an  able  corps  of  assistants,  each  eminent 
as  a  specialist,  has  presented  to  us  a  very  complete  work  upon  Syphilis  and  Chan- 
croid. The  literature  of  recent  years  is  made  tributary  to  this  work.  Bacterio- 
logical researches  are  brought  to  date,  and  the  complexity  of  the  pathological  rela- 
tions of  syphilis  as  here  treated  form  a  most  valuable  feature  of  the  work.  General 
practitioners  will  find  this  volume  especially  helpful  in  the  diagnosis  and  treatment 
of  syphilis  and  those  affections  in  which  it  is  an  essential  factor." — North  Amer- 
ican Practitioner. 

"  As  a  complete  and  systematic  treatise  on  Syphilis  and  Chancroid  this  book  is 
without  a  rival.  It  is  in  every  sense  modern  and  eminently  practical.  An  especial 
feature  of  this  work  is  the  large  number  of  excellently  executed  illustrations.  The 
work  of  the  publishers  has  been  most  creditably  performed." — University  lledical 
Magazine. 

"  This  massive  volume  of  one  thousand  pages  finishes  this,  one  of  the  most  val- 
uable series  of  works  ever  issued  in  America.  The  talented  editor  has  gathered 
around  him  the  greatest  teachers  and  writers  of  the  time  to  aid  him  in  this  under- 
taking, and  the  result  is  a  series  of  works  which  will  stand  unrivaled  for  a  long 
time.  They  are  complete,  comprehensive,  and  exhaustive.  The  noted  publishers 
have  printed  this  in  their  most  excellent  style,  all  the  work  being  first  class  in  every 
particular." — New  England  Medical  Monthly. 


D.  APPLETON  AND   COMPANY,  NEW  YORK. 


■1      I        October,  W99. 


MEDICAL 


HYGIEI^IC    WOEKS 


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AULDE  (JOHN).  The  Pocket  Pharmacy,  with  Therapeutic  Index.  A  resume 
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the  Treatment  of  Emergencies  and  Acute  Diseases.     12mo.     Cloth,  $2.00. 

BARKER  (EORDYCE).  On  Sea-Sickness.  A  Popular  Treatise  for  Travelers 
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BARKER  (FORDYCE).  On  Puerperal  Disease.  Clinical  Lectures  delivered  at 
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the  Practitioner.     Third  edition.     8vo.     Cloth,  $5.00;  sheep,  $6.00. 

BARTHOLOW  (ROBERTS).  A  Treatise  on  Materia  Medica  and  Therapeutics 
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8vo.     Cloth,  $5.00 ;  sheep,  $6.00. 

BARTHOLOW  (ROBERTS).  A  Treatise  on  the  Practice  of  Medicine,  for  the 
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BARTHOLOW  (ROBERTS).  On  the  Antagonism  between  Medicines  and  be- 
tween Remedies  and  Diseases.  Being  the  Cartwright  Lectures  for  the  Year 
1880.     8vo.     Cloth,  $1.25. 

BASTIAN  (H.  CHARLTON).  Paralyses:  Cerebral,  Bulbar,  and  Spinal.  A 
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tions.    Small  8vo,  671  pages.     Cloth,  $4.50. 

BASTIAN  (H.  CHARLTON).  Paralysis  from  Brain  Disease  in  its  Common 
Forms.     With  Illustrations.     12mo,  340  pages.     Cloth,  $1.75. 

BILLROTH  (THEODOR).  General  Surgical  Pathology  and  Therapeutics.  A 
Text-Book  for  Students  and  Physicians.  Translated  from  the  tenth  German 
edition,  by  special  permission  of  the  author,  by  Charles  E.  Hackley,  M.  D. 
Fifth  American  edition,  revised  and  enlarged.     8vo.     Cloth,  $5.00;  sheep,  $6.00, 

BOYCE  (RUBERT).  A  Text-Book  of  Morbid  Histology.  For  Students  and 
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BRAMWELL  (BYROM).  Diseases  of  the  Heart  and  Thoracic  Aorta.  Illus- 
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Figures— in  all,  317  Illustrations.     8vo.     Cloth,  $8.00;  sheep,  $9.00. 

BRYANT  (JOSEPH  D.).  A  Manual  of  Operative  Surgery.  New  edition,  revised 
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BURT  (STEPHEN  S.).  Exploration  of  the  Chest  in  Health  and  Disease.  8vo, 
210  pages.     With  Illustrations.     Cloth,  $1.50. 

CAMPBELL  (F,  R.),  The  Language  of  Medicine.  A  Manual  giving  the  Origin, 
Etymology,  Pronunciation,  and  Meaning  of  the  Technical  Terms  foimd  in 
Medical  Literature.     8vo.     Cloth,  $3.00. 


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(Stddents'  Seeies.)     Cloth,  $3.00. 

CHAUVEAU  (A.).  The  Comparative  Anatomy  of  the  Domesticated  Animals. 
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Lyons  Veterinary  School.  Second  English  edition.  Translated  and  edited 
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lique,  of  Belgium,  etc.   8vo,  1084  pages,with  585  Illustrations.   Cloth,  $7.00. 

CORNING  (J.  L.).  Brain  Exhaustion,  with  some  Preliminary  Considerations 
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CORNING  (J.  L.).  Local  Anaesthesia  in  General  Medicine  and  Surgery.  Being 
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trations.    Small  8vo.     Cloth,  $1.25. 

CURRIER  (ANDREW  F.).  The  Menopause.  A  Consideration  of  the  Phe- 
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8vo.     Cloth,  $7.00. 

DENCH  (E.  B.).  Diseases  of  the  Ear.  A  Text-Book  for  Practitioners  and 
Students  of  Medicine.  With  8  Colored  Plates  and  152  Illustrations  in  the 
text.     8vo.     Cloth,  $5.00;  sheep,  $6.00. 

DEXTER  (FRANKLIN).  The  Anatomy  of  tlie  Peritonaium.  12mo.  With 
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Second  edition,  revised  and  enlarged.     121  Illustrations.    12mo.     Cloth,  $1.50. 

ELLIOT  (GEORGE  T.).  Obstetric  Clinic :  A  Practical  Contribution  to  the  Study 
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EVANS  (GEORGE  A.).  Hand-Book  of  Historical  and  Geographical  Phthisi- 
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EWALD  (C.  A.).  Lectures  on  the  Diseases  of  the  Stomach.  By  Dr.  C.  A. 
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FLINT  (AUSTIN).  Medicine  of  the  Future.  An  Address  prepared  for  the 
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FLINT  (AUSTIN,  Jr.).  Text-Book  of  Human  Physiology;  designed  for  the 
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Imperial  Bvo.     Cloth,  $6.00 ;  sheep,  $7.00. 

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FOSTER  (FRANK  P.).  Illustrated  Encyclopedic  Medical  Dictionary  :  Being 
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